Concise presentation on Fungal Keratitis & HSV

1. Fungal keratitis
Herpes Simplex keratitis
Dr.Pradnya Laddha,
SAANVI EYE CLINIC,Nagpur

2. 
• Complete understanding of fungal keratitis and
Herpes Simplex keratitis
Purpose

3. 
Learning objectives
Sr.
no
Objectives Domain Level
1 To acquire knowledge of Herpes
Simplex keratitis
Cognitive Must know
2 To acquire knowledge of fungal
corneal ulcer
Cognitive Must know

4. 
Fungal isolates have been classified into the following
groups:
 Moniliaceae (nonpigmented filamentary fungi,
including Fusarium and Aspergillus species)
 Dematiaceae (pigmented filamentary fungi,
including Curvularia and Lasiodiplodia species)
 Yeasts (including Candida species
Fungal keratitis-
pathogenesis

5. 
 Fungi gain access into the corneal stroma through a
defect in the epithelium
 Then multiply and cause tissue necrosis and an
inflammatory reaction
 The epithelial defect usually results from trauma (eg,
contact lens wear, foreign material, prior corneal
surgery)
Fungal keratitis-
pathogenesis

6. 
 Topical steroid use has definitively been implicated
as a cause of increased incidence, development, and
worsening of fungal keratitis
 Other risk factors to consider are foreign bodies, and
immunosuppressive diseases
Fungal keratitis-
pathogenesis

7. 
• A history of outdoor eye trauma
Symptoms include the following:
• Foreign body sensation
• Pain or discomfort
• Blurry vision
• Redness
• Watering and discharge
• Photophobia
Fungal keratitis-
presentation

8. 
 Fine or coarse granular infiltrate within the
epithelium and anterior stroma
 Gray-white color, dry, and rough corneal surface
that may appear elevated
 Typical irregular feathery-edged infiltrate
 White ring in the cornea and satellite lesions near the
edge of the primary focus of the infection
Fungal keratitis-
presentation

9. 
In advanced cases
 Suppurative stromal keratitis associated with
conjunctival hyperemia
 Anterior chamber inflammation
 Hypopyon
 Iritis
 Endothelial plaque
 Corneal perforation
Fungal keratitis-
presentation

10. 
Fungal keratitis-
presentation

11. 
 Keratitis, Bacterial
 Keratitis, Herpes Simplex
 Keratitis, Interstitial
 Keratopathy, Neurotrophic
Differential Diagnoses

12. 
 Corneal scrapings are obtained using a platinum
spatula, surgical blade, or calcium alginate swab
inoculated on Sabouraud agar plates
 Gram and Giemsa stains of corneal scrapings have
sensitivities of about 50% in establishing a diagnosis
 Calcofluor white stain (requires a fluorescent
microscope) also can identify fungal organisms.
Fungal keratitis-
investigation

13. 
Fungal keratitis-
investigation
Gram stained Candida

14. 
 Amphotericin B -yeasts
 Natamycin -filamentous organisms
 Azoles (imidazoles and triazoles) include
ketoconazole, miconazole, fluconazole, itraconazole,
econazole, and clotrimazole
Fungal keratitis-
treatment

15. 
Subconjunctival injections may be used in
patients with severe keratitis or keratoscleritis.
They also can be used when poor patient
compliance exists
An oral antifungal (eg, ketoconazole,
fluconazole) should be considered for patients
with deep stromal infection
Approximately one third of fungal infections fail
to respond to medical treatment and may result
in corneal perforation. In these cases, a
therapeutic penetrating keratoplasty is necessary
Fungal keratitis-
treatment

16. 
 HSV is a DNA virus
 Infection occurs by direct contact of skin or mucous
membrane with virus-laden lesions or secretions
 HSV type 1 (HSV-1) is primarily responsible for
orofacial and ocular infections
 HSV type 2 (HSV-2) generally is transmitted
sexually and causes genital disease
HSV keratitis-
Pathophysiology

17. 
 Primary HSV-1 infection occurs most commonly in
the mucocutaneous distribution of the trigeminal
nerve.
 It is often asymptomatic but may manifest as a
nonspecific upper respiratory tract infection
 After the primary infection, the virus spreads from
the infected epithelial cells to nearby sensory nerve
endings and is transported along the nerve axon to
the cell body located in the trigeminal ganglion.
 There, the virus genome enters the nucleus of a
neuron, where it persists indefinitely in a latent state
HSV keratitis-
Pathophysiology

18. 
Recurrence
 Recurrent ocular HSV infection has traditionally
been thought of as reactivation of the virus in the
trigeminal ganglion, which migrates down the nerve
axon to produce a lytic infection in ocular tissue
 Evidence suggests that the virus may also subsist
latently within corneal tissue, serving as another
potential source of recurrent disease and causing
donor-derived HSV disease in transplanted corneas
HSV keratitis-
Pathophysiology

19. 
Causes of the various manifestations :
 Infectious epithelial keratitis - Results from active
viral replication within the corneal epithelium
 Neurotrophic keratopathy - A poorly understood
disease; the cause is thought to be multifactorial
HSV keratitis

20. 
 Necrotizing stromal keratitis - Arises from direct
infection of the corneal stroma and the resultant
severe host inflammatory response ; the use of
topical corticosteroids without antiviral coverage
may be a possible risk factor for its development
HSV keratitis

21. 
 Immune stromal keratitis - An antibody-complement
cascade triggered by retained viral antigen or altered
host antigen within the stroma
 Endotheliitis - Believed to be primarily an
immunologic reaction to an antigen in endothelial
cells; however, the role of live virus has been
speculated
HSV keratitis

22. 
 Pain
 Photophobia
 Blurred vision
 Tearing
 Rednes
HSV keratitis-
presentation

23. 
 Dendritic ulcers
 Geographic ulcer
HSV-epithelial keratitis

24. 
Dendritic ulcers
 This is the most common presentation of HSV
keratitis
 Linear branching pattern with terminal bulbs,
swollen epithelial borders that contain live viruses,
and central ulceration through the basement
membrane
HSV-epithelial keratitis

25. 
Geographic ulcers
 If the infectious ulcer enlarges, its shape is no longer
linear. It is then referred to as a geographic ulcer
HSV-epithelial keratitis

26. 
 Failure of re-epithelialisation due to corneal
anaesthesia
 Persistent epithelial defect
 No pain
 Stroma is opaque and thin
HSV-Neurotrophic
keratopathy

27. 
 Dense stromal infiltrate, ulceration, and necrosis, is
believed to result from viral replication in stromal
keratocytes and severe host inflammatory response
 May lead to thinning and perforation within a short
period
HSV-Necrotizing
stromal keratitis

28. 
 Central zone of stromal edema usually with
overlying epithelial edema
 Surrounding (Wessely) immune ring of stromal haze
 KPs
 Folds in DM
HSV-endotheliitis(disciform
keratitis)

29. 
 Herpes simplex virus (HSV) keratitis remains primarily a
clinical diagnosis based on characteristic features of the
corneal lesion
Tests available:
 Giemsa stain - Scrapings of the corneal or skin lesions
show multinucleated giant cells
 Papanicolaou stain - This shows intranuclear eosinophilic
inclusion bodies
 Viral culture
 Immunohistochemistry looking for viral antigens
 Polymerase chain reaction (PCR) assay
HSV keratitis-investigations

30. 
 Ganciclovir ophthalmic gel 0.15% or Acyclovir 3%
ointment - 5 times daily
 Oral acyclovir 400 mg
 Adequate débridement with a cotton-tipped
applicator
 Steroids for disciform keratitis
HSV keratitis-treatment

31. 
 Fungal keratitis remains a diagnostic and therapeutic
challenge to the ophthalmologist.
 Difficulties are related to establishing a clinical
diagnosis, isolating the etiologic fungal organism in
the laboratory, and treating the keratitis effectively
with topical antifungal agents
 Even if the diagnosis is made accurately,
management remains a challenge because of the
poor corneal penetration and the limited commercial
availability of antifungal agents
Summary

32. 
 Dendritic ulcers are the most common presentation
of HSV keratitis
 The earliest signs of neurotrophic keratopathy
include an irregular corneal surface and punctate
epithelial erosions
 Necrotizing stromal keratitis is characterized by
dense stromal infiltrate, ulceration, and necrosis
Summary

33. 
 Of the 70 different fungi that have been implicated as
causing fungal keratitis, the 2 medically important
groups responsible for corneal infection are yeast
and filamentous fungi
 Since most cases of HSV epithelial keratitis resolve
spontaneously within 3 weeks, the rationale for
treatment is to minimize stromal damage and
scarring
Applied aspect

34. 
 Write pathogenesis, clinical features and
management of fungal keratitis
 Write pathogenesis, clinical features and
management of Herpes Simplex keratitis
Expected questions

35. 
 Prajna NV, Nirmalan PK, Mahalakshmi R, Lalitha P, Srinivasan M.
Concurrent use of 5% natamycin and 2% econazole for the
management of fungal keratitis. Cornea. Nov 2004;23(8):793-6
 Thomas PA. Fungal infections of the cornea. Eye. Nov 2003;17(8):852-
62.
 Wilhelmus KR. Diagnosis and management of herpes simplex stromal
keratitis. Cornea. 1987;6(4):286-91
 Tabbara KF. Treatment of herpetic keratitis. Ophthalmology. Sep
2005;112(9):1640
References

36. 
Thanks