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Bacterial Keratitis - Causes, Symptoms and Treatment

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Bacterial Keratitis –
Causes, Symptoms and Treatment
Hadassah Janumala, Praveen Kumar Sehgal and Asit Baran Mandal
Central Leather Research Institute
India
1. Introduction
The human eye is a complex organ of vital importance for everyday life. Eyes are the parts of
our body that perceive light to see the world and to understand how objects relate to each
other. We can distinguish far objects from close ones and determine their color and shape
(Figure 1). The cornea is the dome-shaped window in the front of the eye. When looking at a
person's eye, one can see the iris and pupil through the normally clear cornea. The cornea
bends light rays as a result of its curved shape and accounts for approximately two-thirds of
the eye's total optical power, with the lens of the eye contributing the remaining one-third. The
cornea is as smooth and clear as glass but is strong and durable (Figure 2). It helps to shield the
rest of the eye from germs, dust, and other harmful matter. The cornea shares this protective
task with the eyelids, the eye socket, tears, and the sclera, or white part of the eye. A very thin
tear film lies between the front of the cornea and our environment. The cornea copes very well
with minor injuries or abrasions. If the highly sensitive cornea is scratched, healthy cells slide
over quickly and patch the injury before infection occurs and vision is affected.
Fig. 1. Structure of the eye
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Fig. 2. Cornea is the clear part of the eye that covers the pupil
Bacterial keratitis is an infection and inflammation of the cornea that cause pain, reduced
vision, light sensitivity and tearing or discharge from the eye that can, in severe cases
cause loss of vision. Bacterial keratitis progresses rapidly and corneal destruction may be
complete in 24 - 48 hours with some of the more virulent bacteria. The severity of the
corneal infection usually depends on the underlying condition of the cornea and the
pathogenicity of the infecting bacteria. It may involve the center of the cornea or the
peripheral part of the cornea (that portion closest to the sclera) or both. Keratitis may
affect one eye or both eyes. Keratitis may be mild, moderate, or severe and may be
associated with inflammation of other parts of the eye (Figure 3). Keratitis can be
classified by its location, severity, and cause. If keratitis involves the surface (epithelial)
layer of the cornea, it is called superficial keratitis. Kerato-conjunctivitis is inflammation
of the cornea and the conjunctiva. Kerato-uveitis is inflammation of the cornea and the
uveal tract, which consists of the iris, ciliary body, and choroid. Keratitis may be acute or
chronic. It may occur only once or twice in an eye or be recurrent. It may be limited in its
effects on the eye or be progressive in its damage. Bacterial keratitis is a sight-threatening
process. Many patients have a poor clinical outcome if aggressive and appropriate
therapy is not promptly initiated. Some cases of keratitis results from unknown factors.
Until recently, most cases of bacterial keratitis were associated with ocular trauma or
ocular surface diseases. Various types of infections, dry eyes, injury, and a large variety of
underlying medical diseases may all lead to keratitis.
Dry eye syndrome (DES; keratoconjunctivitis sicca) is a disorder of the tear film due to tear
deficiency or excessive evaporation, which cause damage to the ocular surface.
(Holly et al., 1977;
Janumala H et al., 2009, 2010; Lemp et al., 1998; Tsubota et al, 1996)
The signs of DES include foreign body
sensation, ocular discomfort (scratchy, dry, sore, gritty, burning sensations) and problems
with visual acuity.
(Stern et al., 1998; Tsubota et al., 1992)
Bacterial keratitis accounts for approximately 65%
to 90% of all corneal infections.
(Marios et al., 2007)
Bacterial Keratitis – Causes, Symptoms and Treatment
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Fig. 3. Human eye with non-ulcerative Bacterial Keratitis
The spectrum of bacterial keratitis can also be influenced by geographic and climatic factors.
Many differences in keratitis profile have been noted between populations living in rural or
in city areas, in western, or in developing countries. Ulcerations of the cornea may occur, a
condition known as ulcerative keratitis. Before the advent of antibiotics, syphilis was a
frequent cause of keratitis. Corneal ulceration, stromal abscess formation, surrounding
corneal edema, and anterior segment inflammation are characteristic of this disease. There
are several types of keratitis, including superficial punctate keratitis, in which the cells on
the surface of the cornea die; interstitial keratitis, a condition that can be either the direct
result of infection, or more commonly secondary to an immunologic process; herpes simplex
viral keratitis, caused by the sexually transmitted herpes virus; and traumatic keratitis,
which results when a corneal injury leaves scar tissue. Early diagnosis and treatment is the
key to minimizing any visual-threatening sequelae. In addition, close follow-up, attention to
laboratory data, and changing antimicrobials if no clinical improvement is evident are
important elements for successful outcome. The severity of the corneal infection usually
depends on the underlying condition of the cornea and the pathogenicity of the infecting
bacteria. Many patients have a poor clinical outcome if aggressive and appropriate therapy
is not promptly initiated.
(Acharya et al., 2009; Tang et al., 2009)
1.1 Epidemiology frequency
The most common predisposing factor for keratitis in southeast Brazil is trauma, especially
corneal injury due to vegetation; observation clearly connected with following risk factors.
The risk of agricultural predominance and vegetative corneal injury in fungal keratitis and
associated ocular diseases in bacterial keratitis increase susceptibility to corneal infection. A
hot, windy climate makes fungal keratitis more frequent in tropical zones, whereas bacterial
keratitis is independent of seasonal variation and frequent in temperate zones. In tropical
countries the incidence of bacterial keratitis is pathogens and show geographical variation in
their prevalence. Thus, the spectrum of microbial keratitis varies with geographical location
influenced by the local climate and occupational risk factors. In United States
Approximately 25,000 Americans develop bacterial keratitis annually. International
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incidence of bacterial keratitis varies considerably, with less industrialized countries having
a significantly lower number of contact lens users and, therefore, significantly fewer contact
lens-related infections. Mortality/Morbidity in cases of severe inflammation, a deep ulcer
and a stromal abscess may coalesce, resulting in thinning of the cornea and sloughing of the
infected stroma.
2. Causes of bacterial keratitis
Keratitis can lead to vision loss from corneal scarring. Physical or chemical trauma is a
frequent cause of keratitis. If the cornea is hit and damaged by a foreign body (a finger nail,
an arm, a metal splinter or through contact lenses), can cause a scratch to the cornea.
Scratches are usually harmless and not very deep, but they give bacteria and viruses the
possibility of attacks, which gives the cornea inflammation and should therefore be detected
and treated. There are various types of keratitis, but most commonly it occurs after an injury
to the cornea, dryness, inflammation of the ocular surface or contact lens wear. A wide
variety of conditions can lead to inflammation of the cornea. Among them are viral,
bacterial, or fungal infections; exposure to ultraviolet light such as sunlight or sunlamps;
exposure to other intense light sources such as welding arcs or snow or water reflections;
irritation from excessive use of contact lenses; dry eyes caused by an eyelid disorder or
insufficient tear formation; a foreign object in the eye; a vitamin A deficiency; or a reaction
to eye drops, eye cosmetics, pollution, or airborne particles such as dust, pollen, mold, or
yeast. The condition is also a side effect of certain medications. Bacterial keratitis remains
one of the most important potential complications of contact lens use and refractive corneal
surgery. "Organisms can infiltrate an intact cornea of a lens-wearer, and a biofilm can form
on the contact lens. Interruption of an intact corneal epithelium and/or abnormal tear film
permits entrance of microorganisms into the corneal stroma, where they may proliferate and
cause ulceration or secondary effect or molecules and cause infection. The epithelium and
stroma in the area of injury and infection swell and undergo necrosis. Acute inflammatory
cells (mainly neutrophils) surround the beginning ulcer and cause necrosis of the stromal
lamellae. The collagen of the corneal stroma is poorly tolerant of the bacterial and leukocytic
enzymes, and undergoes degradation, necrosis and thinning. This leads to scarring of the
cornea. As thinning advances, the cornea may perforate, thus introducing bacteria into the eye
with ensuing endophthalmitis. Corneal infections rarely occur in the normal eye. They are a
result of an alteration in the cornea’s defense mechanisms that allow bacteria to invade when
an epithelial defect is present. The organisms may come from the tear film or as a contaminant
from foreign bodies, contact lenses or irrigating solutions. The severity of the disease depends
on the strain of the organism, the size of the inoculums, the susceptibility of the host and
immune response, the antecedent therapy and the duration of the infection. The process of
corneal destruction can take place rapidly (within 24hrs with virulent organisms) so that rapid
recognition and initiation of treatment is imperative to prevent visual loss.
Contact lens users are at an increased risk of corneal ulcers (Figure 4, Figure 5). The annual
incidence of bacterial keratitis with daily-wear lenses is 3 cases per 10,000. Contact lens is the
leading cause of corneal inflammation, and if we as a contact lens user experience the following
symptoms should seek medical attention right away. The injury may become secondarily
infected or remain noninfectious. Retained corneal foreign bodies are frequent sources of
keratitis. (Dart et al., 1988; Liesegang et al 1997; Moriyama et al., 2008; Musch et al 1983; Poggio et al., 1989; Weissman et al., 2002)
Bacterial Keratitis – Causes, Symptoms and Treatment
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Fig. 4. Contact lens use
Fig. 5. Eye with keratitis infection due to contact lens use
2.1 Other causes for bacterial keratitis are
Disturbances in the tear film may lead to changes in the corneal surface through drying
of the corneal epithelium. This type of keratitis is usually superficial and most
commonly is related to dry eyes and is known as keratitis sicca. If the eyes are
extremely dry, the surface cells may die and form attached filaments on the corneal
surface, a condition known as filamentary keratitis.
Disorders that cause dry eyes; has no or limited germ fighting protection tears causing
ulcers.
Chemical solution splashes can injure the cornea and lead to corneal ulceration.
Ultraviolet light from sunlight (snow blindness), a tanning light or a welder's arc, contact-
lens over wear, and chemical agents, either in liquid form splashed into the eye or in gases
in the form of fumes can all result in non-infectious superficial punctate keratitis,
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Inability to close the eyelids properly can also lead to cornea drying, including
entropion with trichiasis and lagophthalmos a condition termed exposure keratitis.
Allergies to airborne pollens or bacterial toxins in the tears may also cause a non-
infectious type of keratitis. Autoimmune diseases create a similar appearance, often
affecting the periphery of the cornea, termed marginal keratitis or limbic keratitis.
Decreased immunologic defenses secondary to malnutrition, alcoholism, and diabetes
(Moraxella).
Corneal ulcers are commonly caused by bacterial or fungal invasions following superficial
corneal abrasions; among the common infectious agents are: staphyloccus, streptococcus,
herpes (both simplex and zoster), adenovirus, rubeola, rubella, mumps, trachoma, infectious
mononucleosis, and pneumococcus; also at fault may be Vitamin A deficiency or broad -
spectrum antibiotic drug reactions. Corneal ulcers may also follow trauma, may be
associated with other eye infections (e.g., conjunctivitis), may be related to other corneal
disorders (e.g., degenerative conditions, or ptosis, which may cause a "dry eye"), or may
arise from a variety of systemic disorders (especially those of autoimmune origin). In cases
of severe inflammation, a deep ulcer and a stromal abscess may coalesce, resulting in
thinning of the cornea and sloughing of the infected stroma. Once the corneal defenses are
breached, specifically the epithelial glycocalyx, the cornea is prone to infection. Possible
causes include direct corneal trauma, chronic eyelid disease, tear film abnormalities
affecting the ocular surface and hypoxic trauma from contact lens wear. Pathogenic bacteria
colonize the corneal stroma and immediately become antigenic, both directly and indirectly,
by releasing enzymes and toxins. This sets up an antigen-antibody immune reaction that
leads to an inflammatory reaction. The body releases polymorphonuclear leukocytes
(PMNs) that aggregate at the area of infection, creating an infiltrate. The PMNs phagocytize
and digest the bacteria. The collagen stroma is poorly tolerant of the bacterial and leukocytic
enzymes and undergoes degradation, necrosis and thinning. This results in scarring of the
cornea. With severe thinning the cornea may perforate, creating the possibility for
endophthalmitis.
2.2 Gender
Males have a 30 to 40 per cent increased risk of developing keratitis compared to females.
This gender difference has been reported previously for microbial keratitis. The reason for
this association may be related to perceived health risks. Males have different attitudes and
perceptions relating to health risks than do females, whereby they perceive risks as much
smaller and much more acceptable. For example, males may be more inclined to
underestimate the risk of developing corneal infiltrative events (CIE) when sleeping in
contact lenses. (Efron et al., 2005a, 2005b, 2006; Morgan et al., 2005a, 2005b)
2.3 Smoking
Smoking was found to be associated with a 35 per cent greater risk of developing CIE’s and
this was increased to two-fold for severe keratitis. Others have reported similar findings.
Smoking may be a risk factor for a number of reasons. It is generally considered that
smoking is an unhygienic pursuit, which may be linked to a general lack of hygiene with
respect to matters relating to contact lens wear and care. Toxins from smoke may either
irritate the eyes directly or become absorbed into the contact lens and act as an irritant that
Bacterial Keratitis – Causes, Symptoms and Treatment 21
compromises the health of the ocular surface and predisposes the eye to the development of
corneal infiltrative events (CIE). Cigarette smoke is known to have an immuno-modulatory
effect, which may indirectly predispose a cigarette smoker to develop a CIE.
2.4 Ocular and general health
Lens wearers have approximately twice the risk of developing a CIE in the absence of
compromised ocular and general health. The protective effect of compromised ocular health
in lowering the risk of contact lens associated CIEs may be explained by the precautionary
attitude adopted by those with compromised ocular health in that such persons may cease
lens wear, reduce wearing time or use self-prescribed topical ocular medications in an
attempt to alleviate their condition. Such strategies might have the secondary effect of
precluding the development of a CIE. An alternative explanation is that compromised
ocular health may be associated with a general up- regulation of the innate defense status of
the eye, so that there is an ever-present resistance to extraneous challenges to the ocular
surface, which could result in a CIE. These principles can be extended to explain why
compromised general health also serves to protect the eye from developing a CIE.
2.5 Season
The notion that adverse ocular conditions related to contact lens wear can be influenced by the
time of year (seasonal effect) is well established; for example, Begley, Riggle and Tuel reported
that the onset of contact lens-associated papillary conjunctivitis was seasonal, in that the
incidence of this condition peaked during the allergy seasons in mid-western USA. We found
a two to four times increased risk of developing CIEs in late winter (January to March in the
northern hemisphere) compared with mid-summer (July in the northern hemisphere). We
accessed the number of consultations for influenza-like illness to the United Kingdom
National Health Service helpline by people aged 15 to 64 years in England during the same
period as the Manchester Keratitis Study. This number peaked around October and November
2003, which is in disacordance with the peak incidence of CIEs in our study from January to
March 2003. Interestingly, this observation is consistent with the finding of a lower incidence
of CIEs in association with compromised general health. (Efron et al. 2006)
2.6 Risk of keratitis
In the Manchester Keratitis Study (Morgan et al 2005), logistic regression analyses were performed
to investigate the association between a range of risk factors and the occurrence of CIEs.
Daily wear of rigid lenses was found to be associated with a lower risk of developing CIEs
compared with daily wear of hydrogel lenses. The risk of developing CIEs when sleeping in
contact lenses is higher than in daily lens wear.
3. Symptoms of bacterial keratitis
The symptoms of keratitis usually include pain, tearing, and blurring of vision. The pain
may be mild to severe, depending on the cause and extent of the inflammation. Sensitivity
to light may also be present. To the observer, the eye may appear red, watery, and if the
cornea has extensive keratitis, the normally clear cornea may look grey or have white to
grey areas.
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3.1 Physical
External and biomicroscopic examination of these patients reveal some or all of the
following features: Ulceration of the epithelium; corneal infiltrate with no significant tissue
loss; dense, suppurative stromal inflammation with indistinct edges; stromal tissue loss; and
surrounding stromal edema. Increased anterior chamber reaction with or without hypopyon
folds in the descemet membrane. Upper eyelid edema, Posterior synechiae surrounding
corneal inflammation is either focal or diffuse, conjunctival hyperemia adherent
mucopurulent exudate, endothelial inflammatory plaque.
A scratch on the cornea can cause
Light annoyance.
Blurred vision.
Feeling "something in the eye".
Pain
Cornea inflammation with bacteria cause
Your eye turns red.
Pain, impaired vision and sensitivity to light as a scratch.
May be you see a gray-white speck in the eye (the pupil).
The patient will present with a unilateral, acutely painful, photophobic, eye. Visual acuity is
usually reduced, and profuse tearing is common. There will be a focal stromal infiltrate with
an overlying area of epithelial excavation. There is likely to be thick, ropy, mucopurulent
discharge. The cornea will be very edematous. The conjunctival and episcleral vessels will
be deeply engorged and inflamed, often greatly out of proportion to the size of the corneal
defect. In severe cases, there will be a pronounced anterior chamber reaction, often with
hypopyon. Intraocular pressure may be low due to secretory hypotony of the ciliary body,
but most often will be elevated due to blockage of the trabecular meshwork by
inflammatory cells. Often, the eyelids will also be edematous. Bacterial keratitis is a sight-
threatening process. Bacterial keratitis makes the cornea cloudy. It may also cause abscesses
to develop in the stroma, which is located beneath the outer layer of the cornea.
Interruption of an intact corneal epithelium and/or abnormal tear film permits entrance of
microorganisms into the corneal stroma, where they may proliferate and cause ulceration.
Virulence factors may initiate microbial invasion, or secondary effector molecules may assist
the infective process. Many bacteria display several adhesions on fimbriated and non-
fimbriated structures that may aid in their adherence to host corneal cells. During the initial
stages, the epithelium and stroma in the area of injury and infection swell and undergo
necrosis. Acute inflammatory cells (mainly neutrophils) surround the beginning ulcer and
cause necrosis of the stromal lamellae. Diffusion of inflammatory products (including
cytokines) posteriorly elicits an outpouring of inflammatory cells into the anterior chamber
and may create a hypopyon. Different bacterial toxins and enzymes (including elastase and
alkaline protease) may be produced during corneal infection, contributing to the destruction
of corneal substance. The most common groups of bacteria responsible for bacterial keratitis
are as follows: Streptococcus, Pseudomonas, Enterobacteriaceae (including Klebsiella, Enterobacter,
Serratia, and Proteus), and Staphylococcus species.
Bacterial Keratitis – Causes, Symptoms and Treatment 23
3.2 Complications with keratitis
Irregular astigmatism: Another possible complication of these infections is uneven healing
of the stroma, resulting in irregular astigmatism.
Corneal perforation: This is one of the most feared complications of bacterial keratitis that
may result in secondary endophthalmitis and possible loss of the eye.
3.3 How is keratitis diagnosed?
Keratitis can be diagnosed by an ophthalmologist (a physician who specializes in diseases
and surgery of the eye) by physical examination of the eye and history. The history consists
of questions documenting a past medical and ocular history and the symptoms specific to
the current visit. The eye examination will consist of checking the vision and careful
inspection of the corneas using a slit lamp, which is a microscope with excellent illumination
and magnification to view the ocular surface and the cornea in detail. In cases in which
infection is suspected, a culture may be taken from the surface of the eye for specific
identification of the bacteria, virus, fungus, or parasites causing keratitis. Slit lamp
examination helps to diagnose the depth of the keratitis eye infection.
Swab the eye or take samples from the eye to confirm the diagnosis of herpes simplex
infection.
Testing visual sharpness and clearness (visual acuity).
Testing how well the pupil responds to light.
Patients’ history to know about any recent infection of the upper respiratory tract
accompanied by cold sores.
Blood tests may also be done in certain patients with suspected underlying disease.
3.4 What are the risk factors for keratitis?
Major risk factors for the development of keratitis include any break or disruption of
the surface layer (epithelium) of the cornea.
The use of contact lenses increases the risk for the development of keratitis, especially in
poor hygiene, improper solutions, or over wear of the lens.
A decrease in the quality or quantity of tears predisposes the eye to the development of
keratitis due to corneal drying.
Disturbances of immune function through diseases such as AIDS or the use of
medications such as corticosteroids or chemotherapy also increase the risk of
developing keratitis.
3.5 Precautions and complications of corneal inflammation
If you have a job where you are exposed to metal pieces or similar things, you should wear
goggles and visit a doctor when symptoms of a scratch on the cornea appear to prevent
inflammation. Inflammation can spread deeper into the cornea and is difficult to treat.
Therefore we should seek medical advice by herpes cornea inflammation every time.
Bacteria can also produce a severe corneal inflammation, which in the worst case,
permanent visual impairment. You must also not wear contact lenses before the eye has
healed. If the scratch penetrates the cornea more deeply, however, the healing process will
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take longer, at times resulting in greater pain, blurred vision, tearing, redness, and extreme
sensitivity to light. These symptoms require professional treatment. Deeper scratches can
also cause corneal scarring, resulting in a haze on the cornea that can greatly impair vision.
In this case, a corneal transplant may be needed.
4. Treatment of bacterial keratitis
Wound healing of the ocular surface is a special process due to its non-vascularity. It
depends on surrounding corneal tissues for nourishment. Healing requires regeneration of
the corneal and conjunctival epithelium, reduced scar formation, retention of transparency
of cornea and mobility of the conjunctiva. Janumala H et al., 2009; Reim et al. 1997) The process of corneal
wound healing consists of different phases, i.e. latent phase, cell migration, adhesion and
cell proliferation. Another fluoroquinolone, ofloxacin 0.3% (Ocuflox) is also an effective
treatment for bacterial keratitis. Both fluoroquinolones are as effective at managing bacterial
keratitis as fortified antibiotics, but with significantly fewer side effects. (Marios et al., 2007; Baker et
al., 1996) Adjunctive use of cold compresses will also help to reduce inflammation. If there is
evidence of secondary inflammatory glaucoma, Rx a topical beta-blocker BID. Have the
patient return daily for follow-up visits. Once the infection is controlled, add a topical
steroid Q2H to the regimen. Continue the daily follow-up and begin to taper all medications
as you see improvement. (McLeod et al., 1995)
4.1 What is the treatment for keratitis?
Medical treatment is absolutely essential - even a delay of a few hours can affect the ultimate
visual result. The causative factors must be determined through laboratory analysis of
scrapings; medical treatment (i.e., medication) varies according to the cause. As with
bacterial conjunctivitis, culturing the infection is the ideal way to determine the infecting
organism but is often difficult or impractical. First and foremost, you must halt bacterial
proliferation; do not delay treatment while waiting for the culture results. If you have the
materials available, scrape the ulcer using a platinum spatula and plate the specimen into
blood and chocolate agar culture media. A simpler but less effective method is to use a
culturette. (McLeod et al 1996; Miedziak et al., 1999; Schaefer et al., 2001) Regardless, immediately begin therapy
with a broad - spectrum antibiotic. A popular initial therapy is the fluoroquinolone
ciprofloxacin 0.3% (Ciloxan) two drops every 15 minutes for six hours, followed by two
drops every 30 minutes for 18 hours, and then tapered depending on patient response.
Infectious keratitis generally requires antibacterial therapy to treat the infection. This
treatment can involve prescription eye drops, pills, or even intravenous therapy. Any
corneal or conjunctival foreign body should be removed. Wetting drops may be used if
disturbance of the tears is suspected to be the cause of the keratitis. Steroid drops may often
be prescribed to reduce inflammation and limit scarring. This must be done carefully and
judiciously, since some infections can be worsened with their use. Treatment depends
largely on the source of the problem. If a common adenoviral virus is causing the keratitis,
the condition is likely to clear up on its own, usually in about two to three weeks. Available
medications for this form of keratitis include palliative treatment. Contact-lens wearers are
typically advised to discontinue contact-lens wear, whether or not the lenses are related to
the cause of the keratitis.
Bacterial Keratitis – Causes, Symptoms and Treatment 25
4.2 Treatment of scratches on the cornea
Foreign body should be removed if it sits in the eye.
Antibiotics-drops to prevent inflammation.
Possibly putting a small bandage over the eye in order to give it a little calm.
4.3 Keratitis antibiotic treatment
Staphylococcus aureus is a major cause of bacterial keratitis. (Alexandrakis et al., 2003; Liesegang et al. 1998)
S. aureus ocular infections can cause severe inflammation, pain, corneal perforation, scarring,
and loss of visual acuity. (Chusid et al., 1979) S. aureus has a long history of evolving to more resistant
states, and this trend is expected to continue. (Hiramatsu et al., 1997; Peterson, 1999) Therefore, new
antibiotics and new antibiotic formulations are needed to manage future cases of S. aureus-
induced keratitis. Moxifloxacin and gatifloxacin are “fourth generation” fluoroquinolone
antibiotics that target bacterial DNA gyrase (topoisomerase II) and topoisomerase IV. (Adams et al.,
1992; Dalhoff et al., 1996; Kato et al., 1992; Shen, 1994) These fourth generation fluoroquinolones have in vitro
activity similar to that of ciprofloxacin and ofloxacin (extended-spectrum fluoroquinolones)
against gram-negative bacteria but enhanced activity against gram-positive bacteria, including
S. aureus. (Biedenbach et al., 1996; Davis et al. 1994) A broadspectrum antibiotic may prevent secondary
bacterial infection. Chronic dendritic keratitis may be effectively treated with vidarabine, long
term topical therapy may be necessary. Keratitis due to exposure requires application of
moisturizing ointment to the exposed cornea and protects it with eye patch. Severe corneal
scarring may be treated by keratoplasty (cornea transplantation). Slit lamp photography can be
useful to document the progression of the keratitis, A B-scan ultrasound can also be carried out
in severe corneal ulcers with no view of the posterior segment. The fourth-generation
ophthalmic fluoroquinolones include moxifloxacin and gatifloxacin and they are now being
used for the treatment of bacterial conjunctivitis. Both antibiotics have better in vitro activity
against gram-positive bacteria than ciprofloxacin or ofloxacin. Moxifloxacin penetrates better
into ocular tissues than gatifloxacin and older fluoroquinolones; in vitro activity of moxifloxacin
and gatifloxacin against gram-negative bacteria is similar to that of older fluoroquinolones.
Polymicrobial keratitis has been reported in up to 12% of cases and can be difficult to treat. The
use of multiple antibiotics simultaneously and with frequent dosing may result in added
toxicity and damage to the ocular surface epithelium, thereby impairing recovery.
Demonstration of broad-spectrum efficacy, excellent safety profiles in ocular infections, and a
distinct mode of resistance acquisition. Moxifloxacin is a fourth-generation fluoroquinolone that
exhibits a broad spectrum of bactericidal activity against both Gram-positive and Gram -
negative bacterial pathogens, including staphylococci, S. pneumoniae, members of the family
enterobacteriaceae, P. aeruginosa, H. influenzae, and Moraxella species. Moxifloxacin also has
better mutant prevention characteristics than other fluoroquinolones. Moxifloxacin has also
been shown to have superior activity compared with ciprofloxacin against quinolone resistant
strains of S. aureus. Data also shows superior corneal and aqueous penetration of moxifloxacin
(Solomon R, Donnenfeld E, et al.) Penetration of topically applied gatifloxacin 0.3%, moxifloxacin 0.5% and
ciprofloxacin 0.3% into the aqueous humor.
4.4 Treatment with Succinylated Collagen Bandage lenses (SCBL)
Succinylated Collagen Bandage Lenses SCBL, are prepared with modified collagen (pH7.4) a
natural biopolymer with biocompatibility with the human cornea, bioerodability, non-
immunogenicity, high oxygen permeability, good water content, optimum thickness and
Keratitis
26
superior physiological environment compared to hydrogel lenses. When used as a corneal
adjunct in various conditions SCBL eliminates side effects such as irritation of the cornea,
inflammation, watering, reduced visual acuity etc. SCBL shows promise to treat dry eyes,
keratitis and epithelial trauma. (Janumala H et al.,2008, Janumala H et al., 2009)
4.5 Complications of keratitis?
Superficial keratitis involves the superficial layers of the cornea and commonly does not lead
to scarring. More extensive keratitis involves deeper layers of the cornea, and a scar may
develop upon healing. This will affect the vision if the central portion of the cornea is involved.
With severe ulcerative keratitis, the cornea may perforate, which is an extremely serious
situation. With proper diagnosis and appropriate treatment including follow-up care, keratitis
can usually be managed without causing permanent visual disturbances. (Callegan et al., 1992; Davis et
al. 1978) Vision often improves with treatment of the underlying infection. However, there may
be some scarring of the cornea after treatment that may or may not affect vision in the long
run. If the corneal scarring is in the center of the cornea, where it affects the line of site, a
corneal transplant may ultimately be needed to improve the vision.
4.6 Can keratitis be prevented?
The risk of keratitis can be reduced through the use of safety precautions to avoid eye
injury, and the prompt treatment of early ocular symptoms.
Many forms of keratitis can be prevented by good hygiene.
Protecting the cornea from injury is the first step, since keratitis also results from a
corneal injury.
If you have a cold sore or genital herpes, avoid touching the eyes.
Have well balanced diet, including vitamin A rich foods such as carrots, squash,
mangoes, sweet potatoes and spinach.
4.6.1 Prevention tips for contact lens users
Contact lens users should always use sterile lens cleanser and disinfection solution.
Do not over use contact lenses at night and make the eyes red or irritated.
Never sleep with the contact lenses in the eyes.
Always store the lenses in disinfecting solutions overnight.
Regularly clean your contact lens case.
Careful contact-lens care including proper cleaning of contact lens cases.
4.6.2 Keratitis home remedies
A sterile, cotton-tipped applicator may be used to gently remove infected tissue and
allow the eye to heal more rapidly.
Can wear an eye patch to protect it from bright light and foreign particles.
Minor infections are treated with antibacterial or antifungal eye drops.
If keratitis is caused by dry eye, artificial tears for lubrication are effective.
Vitamin supplementation such as vitamin A can be used in case deficiency is a
suspected cause.
Bacterial Keratitis – Causes, Symptoms and Treatment 27
4.7 Clinical pearls
If a patient presents with a corneal infiltrate but no overlying epithelial staining, the
condition is not bacterial keratitis. If there is epithelial breakdown but only minor
inflammation and anterior chamber reaction, then it is most likely not infectious
bacterial keratitis.
The inflammatory reaction is as damaging to the cornea as the infective organism. Once
you've halted bacterial proliferation, be sure to prescribe a steroid to speed healing and
reduce corneal scarring. For steroids to be beneficial, they must be used while the ulcer
bed is still open, usually within the first 24 to 48 hours. If you wait until the ulcer re-
epithelializes before adding a steroid, the beneficial effects will be lost.
5. Conclusion
It is extremely important to treat keratitis before corneal tissue is destroyed and scar
tissue is formed. Because the pain is so severe in keratitis, the patient usually welcomes
medical attention. However, if the cornea loses its sensitivity (as in trauma, surgery, or
damage to the trigeminal nerve), ulcers can develop without accompanying pain.
The implications for personal hygiene are evident, especially with children. Hand
washing during periods of illness and following toileting is of vital importance as a
preventive measure.
6. Acknowledgements
I thank Dr. A. B. MANDAL, Director, CLRI-CSIR for his support to publish this book
chapter. I am thankful to my husband Dr. Victor B. Kassey and my loving children Sharon
Kassey, Angela Kassey and Daniel Kassey for their unconditional love, support and
encouragement. Above all, I thank God for "He has made everything beautiful in its time"
(Ecclesiastes 3:11).
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ObjectiveTo study the distribution, current trends, and patterns of resistance to antimicrobial agents of bacterial keratitis isolates in South Florida.DesignRetrospective, observational, case series.ParticipantsThe microbiology records of all patients with bacterial keratitis seeking treatment at the Bascom Palmer Eye Institute from January 1, 1990 through December 31, 1998 were reviewed.Main outcome measuresIn vitro laboratory minimum inhibitory concentration testing of the corneal isolates to the fluoroquinolones (ofloxacin and ciprofloxacin) and to the aminoglycosides (tobramycin and gentamicin) was performed using the Vitek (Automatic Microbial System Biomerieux Vitek, Inc., Hazelwood, Missouri) method.ResultsDuring this 9-year period, 2920 consecutive corneal cultures were obtained, and a pathogen was recovered in 1468 cultures (50%). The number of corneal ulcers scraped, positive cultures, recovered bacterial isolates, and ratio of gram-positive to gram-negative isolates per year remained approximately equal throughout the study period. Staphylococcus aureus and Pseudomonas aeruginosa represented 19.4% and 25.7%, respectively, of the total bacterial isolates during this period. However, we documented a gradual increase in the number of S. aureus keratitis isolates (29% of gram-positive organisms in 1990 versus 48% in 1998, P = 0.01) coupled with a decrease in the number of P. aeruginosa isolates (54% of gram-negative organisms in 1990 versus 46% in 1998). A decrease in the incidence of contact lens-associated keratitis and P. aeruginosa isolates in this group of patients was documented. Serratia marcescens and P. aeruginosa were most commonly isolated in contact lens-associated keratitis (18% each). There was increasing laboratory resistance of S. aureus keratitis isolates to the fluoroquinolones (11% in 1990 to 28% in 1998), but resistance patterns to the aminoglycosides remained unchanged. There was a three-fold increase in the percentage of resistant S. aureus isolates to fluoroquinolones between 1990 and 1994 and between 1995 and 1998. Both fluoroquinolones and aminoglycosides exhibited low in vitro effectiveness against P. aeruginosa throughout the study period.ConclusionsThe increased recovery of S. aureus keratitis isolates and decreased laboratory effectiveness against fluoroquinolones to these pathogens present an important therapeutic challenge.
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The global trend of increasing tolerance and outright resistance to penicillin among streptococcal species becomes even more problematic when considering the coresistance patterns to other commonly used alternative therapies. Levofloxacin is a fluoroquinolone with excellent bioavailability properties that affords potential use in the treatment of a wide variety of infections caused by Gram-positive organisms such as streptococci. We evaluated the antistreptococcal activity (350 strains) of levofloxacin compared with other fluoroquinolones, β-lactams (penicillin and cephalosporins), erythromycin, and vancomycin against β- and α-hemolytic streptococci including penicillin-resistant strains of pneumococci and species within the viridans group. With the exception of one strain, all isolates were inhibited by levofloxacin concentrations of ⩽2 μg/ml including all penicillin-resistant viridans group and pneumococcal strains. This activity was superior to that of comparison fluoroquinolones, all β-lactams, and erythromycin, whereas all strains remained susceptible to vancomycin. Time-kill results established that levofloxacin is bactericidal against most streptococci and has enhanced activity when combined with gentamicin. These results suggest that levofloxacin alone or in combination with an aminoglycoside may prove useful as an alternative to conventional therapeutic approaches of commonly encountered or serious streptococcal infections.
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Wound healing of the corneal is closely associated with the regeneration of the epithelium. It may be impaired by mechanical or chemical damage to the basement membrane, under infections, and in neuroparalytic conditions. Eye burns show such damage. Therefore, experimental models of alkali burns were widely used to investigate wound healing of the ocular surface. Mediators of inflammation play an important part in disease and healing processes. High amounts of inflammatory mediators inhibit the regeneration of the epithelium and induce ulceration. Then, serine and metalloproteinases are released on the ocular surface and inside the tissues. These enzymes melt the stromal matrix. Especially when leukocytes are present, superoxides also appear and destroy the organic substrates of tissues. Therefore, therapeutical support of wound healing on the ocular surface has to take into account many factors. It seems that rather a polyvalent therapy may have a better chance of success. As soon as the epithelial cover is completely closed, stromal wounds heal better, and sometimes inflammation subsides.