common corneal infection

1. Dr. K. Vasantha M.S., F.R.C.S., Edin
Director RIO Chennai (Rtd)

2. Bacterial keratitis implies any form of corneal
inflammation either superficial, interstitial or
deep caused by bacteriae
When this inflammation is accompanied by a
loss of epithelium, it is termed a Corneal Ulcer.

3.  Gram positive bacteriae : Staphylococcus aureus,
epidermidis and others
 Streptococcus pneumoniae. Viridans, pyogenes
 Corynebacterium
 Enterococcus
 Bacillus species
 Propionibacterium acnes
 Micrococcus spp, Peptostreptococci, Clostridium
perfringens

4.  Pseudomonas aeruginosa
 Neisseria species
 Haemophilus species
 Moraxella species
 Serratia marcescens
 Proteus sp., Acinetobacter sp., Enterobacter sp, E.
coli,
 Klebsiella sp., Eikenella sp.
 Pasteurella multocida, Xanthomonas sp.,

5.  Aerobic, nonfermenting gram negative rods
Achromobacter xylosoxidans and Stenotrophomonas
maltophilia are important causes for contact lens
induced keratitis. These are resistant to fluoroquinolones
and aminoglycosides
 Actinomycetes including Nocardia are common in
developing countries
 With orthokeratology lenses Pseudomonas, S.aureus,
Acanthamoeba and Stenotrophomonas are found

6. Normally the epithelium protects the cornea from getting infected.
But these bacteriae can penetrate the epithelium
 Neisseria gonorrhoeae, Neisseria meningitidis
 Corynebacterium diphtheriae
 Haemophilus aegypticus
 Listeria species

7.  Ulcers can occur as secondary infection from the
conjunctival commensals, from the lids or from the sac
when it is inflamed. This will happen when there is an
abrasion. This is the reason why when there is a chronic
dacryocystitis it must be immediately dealt with
 Diabetes and immuno suppressives will also predispose
the person to infection
 Contact lens wear

9.  Watering, pain and redness usually following injury.
 Defective vision. More if the ulcer is in the center
 Lid edema, muco purulent discharge
 Circum corneal congestion, sometimes conjunctival
congestion also. Chemosis if there is severe
inflammation
 Opacity in the cornea which will take up fluorescein stain
as the epithelium will be abraded.

10.  Pupil will be constricted and sluggishly reactive due to
irritation to the iris.
 This toxic reaction can produce hypopyon which will be
sterile in bacterial ulcer.
 In fungal ulcer fungal hyphae may be present.
 Injury with vegetative matter should make one suspect
fungal etiology
 If chronic dacryocystitis is present Pneumococcal
infection must be thought of

11.  Stage of progressive infiltration
 Stage of active ulceration
 Stage of regression
 Stage of cicatrization

12. Characteristics
• Suppuration is the hallmark
•Yellow – white, oval, densely opaque ulcer with relatively clear
surrounding cornea with or without hypopyon
•Two types of stromal infiltration:
•- small, discrete, peripheral anterior stromal infiltrates (free of
replicating bacteria)
•- large, severe, central stromal infiltrates (replicating bacteria
present)
•Tissue damage irreversible and leads to permanent scarring

14.  Often seen when chronic dacryocystitis is present
 Suppuration and cicatrization are seen together. Ulcer
progresses on one side when the other side is healing.
 Hypopyon will be present as this causes severe
iridocyclitis
 See the sutures made for sac
excision

17.  Irregular ulcer with thick greenish mucopurulent
exudate and ground glass appearance of surrounding
cornea (mushy/soupy stroma)
 Presence of hypopyon
 Rapid course – liquefactive necrosis, Descemetocoele
and perforation in 1 or 2 days
 Most common pathogen in bacterial keratitis
associated with contact lens wear

18.  This is a commensal organism present on the skin and
conjunctiva
 Opportunistic infection
 Usually causes secondary infection on HSV keratitis, or
on bullous keratopathy
 Here the ulcer is on a
leucoma

19.  Usually uniocular, mild, paracentral or perilimbal
 Central grey infiltrate – ulcer with grey membranous
base
 Second area of infiltration around it in the deep layers
of stroma with clear area in between
 Infiltrated margin lacking and remaining cornea
relatively clear

21.  Commonest cause is Streptococcus viridans
 Other etiologic agents: like
 Staph. epidermidis, Pseudomonas, Mycobacteria,
Enterococci , Strep. pneumoniae , Peptostreptococcus
and Haemophilus also can rarely cause crystalline
keratopathy
 Serratia marcescens also will give raise to satellite
lesions

22.  Corynebacterium also can cause ulcer in preexisting
corneal lesions
 Bacillus species will cause a rapidly progressing ulcer.
There will be a ring infiltrate remote from the site of
injury
 Enterobacteriaceae will give raise to a shallow ulcer
with grayish white pleomorphic suppuration opaque
stroma and ring infiltrates -> ->

23. When you see an ulcer the following tests must done to
find the causative organism
 Smear
 KOH suspension
 Culture
 Detection of antigens, antibodies and endotoxins
 Immunoglobulins
 PCR
 Confocal microscopy – not possible to see bacteriae as
they are only 0.5 microns in size

24.  Apply topical anesthetic and wait for 3 – 5 mins for the
anesthetic to drain off
 Remove the purulent material with a cotton swab and
discord
 Use a Kimura’s spatula or a surgical blade to take the
sample. This is preferably done under a slit lamp. The
spatula can be sterilized with flame or 70% alcohol.
Contamination by eye lashes is avoided by using a
speculum
 Immediate transfer needed due to small sample

25.  Gram stain: for bacteria, yeasts, cysts of Acanthamoeba.
Can detect 60 – 70% of bacteriae. Fungal hyphae are
Gram negative or faintly stained walls with unstained
protoplasm
 Giemsa: viral and Chlamydia inclusion bodies,
polymorphs and mononuclear cells besides the above
microbes
 Ziehl-Neilson: Mycobacteria and Nocardia
 Acridine orange: bacteria, fungi and Acanthamoeba
cysts

27.  Blood agar: for aerobic bacteriae and fungi esp.
Fusarium
 Chocolate agar: Haemophilus, Neissaria and Moraxella
 Sabouraud’s dextrose agar: fungus
 Thioglycollate broth: both aerobic and anaerobic
 Non nutrient agar with E. coli – Acanthamoeba
 Thayer Martin agar: to isolate Neisseria
 Brain heart infusion: filamentous fungi and Yeast
 Lowenstein Jenson for Mycobacteria

28. Not satisfactory because of
 Small sample
 Prior antibiotic use
 Many organisms are difficult to grow – Streptococci and
Propionibacterium
 Polymicrobial keratitis can occur. It is difficult to
differentiate this from contamination
So while specificity is satisfactory sensitivity is poor

29.  Elisa for detecting different antigens
 Serological tests for IgG and IgM to detect viruses and
Microsporidia
 Limuluslysate test: to detect endotoxins
 Eubacterial PCR is done for all bacteriae

30.  A DNA sequence determination is coupled with
bioinformatic analysis to detect matches between the
sample and a data base of reference genome sequence.
 Rapid and highly accurate identification is possible

31. Aim of the treatment
 To reduce the number of organisms as much and as
quickly as possible
 To reduce the detrimental changes to the cornea caused
by the inflammation

32.  Atropine eye drops are given to cause dilatation and
cycloplegia. This will reduce pain as ciliary spasm which
is the cause for the pain is relieved
 Dilatation will break any synechiae and also prevent
further synechiae from forming
 Atropine reduces the tear secretion and there by
increases the lysozomal content of the tears
 It also separates the corneal lamellae and helps in
penetration of the drops applied

34.  If chronic dacryocystitis is present sac excision has to
be done
 As diabetes may predispose to infection and delay
healing, this must be checked for
 History must be taken regarding use of
immunodepressants and immunosuppression

35.  Broad spectrum fortified antibiotic drops like
Gentamycin and Tobramycin for gram negative
organisms
 Cefuroxime 500 mg in 2 ml if mixed with 8 ml of tear
substitute will give a fortified i.e. 50 mg in one ml
solution
 Loading dose for the first half an hour or so and then
every hour initially
 Once healing starts it can be tapered a little but not like
steroids as tapering might cause resistance

36.  Has a broad spectrum – even against penicillin and
methicillin resistant bacteriae
 Acts against anaerobes and atypical mycobacteriae
 Has a higher solubility than the earlier antibiotics
 Minimum concentration needed is low
 It is bactericidal
 Toxicity and allergenicity are low

37.  Moxifloxacin is less active against Pseudomonas but
more active against Mycoplasma than Gatifloxacin. It is
less likely to give raise to resistance as two mutations
are needed. Moxifloxacin is self preserved and hence
preservatives are not needed
 Since it reaches a higher concentration in the anterior
chamber development of mutation are prevented
 Gatifloxacin acts against even Chlamydia and
Mycoplasma

38. Recommended drugs Alternative drugs
No organism Cefuroxime +
Tobramycin
or
Ciprofloxacin
Bacitracin
Gentamicin
Ofloxacin
Gram positive cocci Cefuroxime Bacitracin
Vancomycin +
Tobramycin
Gram negative
cocci
Cefuroxime Ciprofloxacin
Fortified Ceftriaxone
Gram negative
bacilli
Tobramycin
or
Ciprofloxacin
Gentamicin
Ofloxacin
Gram negative
diplobacilli
(Moraxella sp.)
Cefuroxime
or
Ciprofloxacin
Fortified Ceftriaxone
Ofloxacin

39. Antibiotic Concentr
ation
available
Diluent
(ml)
Final
concent
ration
Shelf
life
Amikacin 1gm/4ml 16 50mg/ml 30 days
Ampicillin 250mg 5 50mg/ml 4hrs
Bacitracin 50,000 U 5 10,000
U/ml
7days
Carbenicillin 1gm 10 100mg/ml 3days

40. Antibiotic Available
conc
Diluent
(ml)
Final
conc
Shelf life
Cefuroxime 500mg 8 50mg/ml 4days
Gentamycin 80mg/2ml 2 20mg/ml 30days
Penicillin
G-K
10million
units
10 1 lakh
U/ml
4days
Polymyxin
B
5 lakh units 10 50,000
U/ml
3days
Tobramycin 80mg/2ml 2ml 20mg/ml 30 days

41. Antibiotic Available
concentrati
on
Diluent
(ml)
Final
concentrati
on
Shelf
life
Vancomycin 500mg 10 50mg/ml 4days
Methicillin ,
Moxalactam
1gm 20 50mg/ml 4days
Cefamandole 500mg 10 50mg/ml 4days
Chlorhexidine 0.2% w/v
(2mg/ml)
5.6ml 0.3mg/ml

42. Active healing

43.  Symptoms will be less
 Congestion will be less
 The ulcer will stop progressing
 The edges will become rounded
 Hypopyon will disappear
 The cornea around the ulcer will become clearer as the
edema comes down

44.  Compliance must be checked
 Change the antibiotics if it is different as per the culture
report
 It must be remembered that with the small sample we get
with ulcers the results may not be accurate
 Resistance to even fluoroquinolones are developing
 Decision regarding therapeutic keratoplasty must be
taken before the ulcer reaches the peripheral cornea

45.  Even when an ulcer heals a scar is produced which will
cause defective vision
 A small peripheral scar may not affect vision .
 If the scar is central mechanical obstruction to vision is
caused.
 A nebular opacity or a peripheral opacity especially one
with iris adherence can cause astigmatism and affect
vision

50.  An ulcer may perforate as the stroma dissolves due to
infection and by the action of neutrophils
 If the perforation is in the periphery the iris plugs the
leak and the ulcer may heal with an adherent leucoma
 If the perforation is in the center a fistula will form. When
this ulcer heals an anterior polar cataract may form
 Sometimes if a small ulcer perforates it may help in
healing as it acts like a paracentesis

51.  Before the ulcer perforates the Descemet’s membrane
will with stand for some time as it is elastic. This will
cause the membrane to bulge forward giving raise to
Descemetocoele
 At this stage and for small perforations glue with either
bandage or bandage contact lens can be used to seal the
perforation
 Glue has a mild antibiotic activity
 It also blocks the neutrophils which causes further
necrosis

53.  If the ulcer progresses further it will become a total ulcer.
A therapeutic keratoplasty must be done if the ulcer is
progressing fast. A rim of normal cornea will give a
better result. So TKP should be done before the ulcer
progresses to involve the peripheral cornea
 Since the eye is inflamed the chances for getting a clear
graft is poor. There is a danger of the infection occurring
in the graft also
 Since large grafts will be needed rejection and glaucoma
are more common

54.  If the infection involves all the layers of the eye it is
called panophthalmitis. Once this happens the eye may
have to be eviscerated. If the infection is controlled at
this stage the eye will become phthisical.