Ocular Herpes Virus: Pathogenesis, Mechanism of Action, and Clinical Features

 
Dr Sanjeev  Kumar Mittal
Professor & Head, Ophthalmology
13-02-2018
 
HERPES VIRUS
HERPES VIRUS
 
Are ubiquitous human pathogen capable of  causing both
asymptomatic  infection and active disease
Humans are natural reservoir of HSV
2 types – HSV 1- oropharynx
 
       
 
        
HSV 2 – genital area
Ocular disease typically caused by type  1
Causes primary infection in children and neonates
 
MODE OF INFECTION:
MODE OF INFECTION:
 
IP – 3- 9 days
HSV 1 – close contact
HSV 2 – venereal – birth canal
 
 
 
MECHANISM OF ACTION
MECHANISM OF ACTION
 
 HSV  
(epitheliotropic & cytolytic)
 binds to one or
more
 
cellular receptor – heparin  sulphate
Virus fuses with cell membrane
Enters the cell and nucleus where the transcription  of
viral DNA occurs – protein
 
TG is the most common source of recurrent HSV infection.
Primary infection may subsequently reactivate by travelling via
 ophthalmic division of 5
th
 CN to the eye.
 
PATHOGENESIS
PATHOGENESIS
 
 
 
Factors for reactivation
Factors for reactivation
 
 
UV rays
Trauma
Heat, abnormal body temperature
Other infectious disease
Emotional disease
Menstrual stress
Steroids, immunosuppresant, PGs
 
CLINICAL FEATURES
CLINICAL FEATURES
 
Suspicion of viral keratitis arises if there is
Suspicion of viral keratitis arises if there is
Associated skin lesions, recurrences of these lesions
Stress-induced recurrence
Immuno compromised status
History of contact
Symptomatic
 
eye (
Pain ,Photophobia ,Blurred vision,
Tearing ,Redness)
 with minimal conjunctival and
corneal signs
Superficial dendrites with loss of corneal sensation
 
CLASSIFICATION OF OCULAR DISEASE
CLASSIFICATION OF OCULAR DISEASE
 
1.Congenital & Neonatal
1.Congenital & Neonatal
 
2
. Primary infection
. Primary infection
 
3. Recurrent infection
3. Recurrent infection
 
CONGENITAL AND NEONATAL OCULAR HERPES
CONGENITAL AND NEONATAL OCULAR HERPES
 
May be acquired by one of the three periods :
May be acquired by one of the three periods :
Intrauterine (5%)
Peripartum(10%)
Postpartum (85%)
 
Intrauterine infection 
occurs in 1/300,000 births, with features of
microophthalmia, retinal dysplasia, optic atrophy and
chorioretinitis.
 
HSV infections in latter two periods are further classified as 
skin,
eyes, or mouth (SEM)
 with or without the other involvement seen
in intrauterine infections.
Ocular herpes include one or all: conjunctivitis, epithelial keratitis,
stromal immune reaction, cataract, necrotizing chrioretinitis.
 
PRIMARY INFECTION
PRIMARY INFECTION
 
After 6 months – maternal anti-HSV IgG
Cutaneous involvement
Cutaneous involvement
vesicular periocular  skin
eruptions , vesicular ulcerative blepharitis
Acute follicular conjunctivitis
Acute follicular conjunctivitis
Keratoconjuctivitis
Keratoconjuctivitis
 
 
with non-suppurative
lymphadenopathy
Diffuse punctate keratitis 
Diffuse punctate keratitis 
– that evolves into
 
multiple
scattered micro dendrite figures.
As a rule confined to epithelium clinically – d/t lack
As a rule confined to epithelium clinically – d/t lack
of previous  immunologic  stimulus
of previous  immunologic  stimulus
 
Treatment-Topical antivirals supported by
  
antibiotics & cycloplegics
 
RECURRENT INFECTION
RECURRENT INFECTION
 
Patients with recurrent herpes have both cellular and
humoral immunity against the virus.
 
corneal vesicles
 
 dendritic ulcer
 
geographic
ulcer(amoeboid)
 
limbal ulcer
(marginal)
 
CLASSIFICATION OF HSV KERATITIS
CLASSIFICATION OF HSV KERATITIS
 
The disease may present as
any one or a combination of
the following:
1
. Blepharoconjuctivitis
. Blepharoconjuctivitis
2. 
Episcleritis, scleritis
Episcleritis, scleritis
3
. Infectious epithelial
. Infectious epithelial
keratitis 
keratitis 
–(IEK)
–(IEK)
4
. Neurotrophic
. Neurotrophic
keratopathy
keratopathy
 
5. 
Stromal keratitis
Stromal keratitis
   
Necrotizing stromal keratitis
    Immune (interstitial) keratitis
    Immune rings
    Limbal vasculitis
    Disciform keratitis
 
    6. 
Endothelitis
Endothelitis
        
Disciform
        Diffuse
        Linear
    7. Iridocyclitis
    7. Iridocyclitis
    
8. Trabeculitis
8. Trabeculitis
 
Herpes simplex epithelial keratitis
 
  Dendritic ulcer with terminal bulbs
 
  Stains with fluorescein
 
  May enlarge to become geographic
 
  Aciclovir 3% ointment  x 5  daily
 Ganciclovir ophthalmic gel 0.15% - 5 times daily
 Supported by antibiotics and cycloplegics
 
  Debridement if non-compliant
 
Treatment
 
I
n 
herpes, corneal sensation is reduced in approx 70 % of the patient.
 
MC PRESENTATION
 
2-3wks
 
  
  
D/D OF DENDRITIC KERATITIS
D/D OF DENDRITIC KERATITIS
 
Herpes zoster dendritic keratitis (pseudodendrites)
 
• Acanthamoeba keratitis
 
• Contact lens keratopathy
 
• Antiviral toxicity
 
 
Herpes simplex disciform keratitis
 
  Central epithelial and stromal oedema
 
  Folds in Descemet membrane
 
  Small keratic precipitates
 
- 
topical steroids
 (pred 1% or dexa 0.1%)
+
 with antiviral cover
 
  Occasionally surrounded by
    Wessely ring
 
Treatment
 
Signs
 
Associations
 
COTND….
 
Oral
 (in immunodeficient or children)
:: Acyclovir 400 mg PO 5t/d * 14 days, or
::Famcyclovir  500 mg PO twice daily for 14 days, 
or
:: Valacyclovir 500 mg PO twice daily for 14 days, or
 
Neurotrophic keratopathy
Neurotrophic keratopathy
( Metaherpetic)
( Metaherpetic)
 
 
Damage to
 
gasserian
ganglion
Impaired corneal
innervations
Decreased tear secretion
Excess use of antivirals
Signs –
Irregular cornea with loss
 
of
corneal lustre
Characterized by persistent
epithelial defect
Oval in
 
shape with gray,
thickened smooth borders
 
Rx-
Stop all unnecessary medications
Gentle debridement of  boggy epithelium
Artificial tears
Mild steroid :If active stromal keratitis +ve
Therapeutic soft CL
Doxycycline 100mg
 
PO once daily to inhibit
collagenase
Cycloplegics: if iritis is +ve
Tarsorrhaphy to treat chronic exposure
Cyanoacrylate glue – if perforation occurs
 
PRIMARILY A CLINICAL DIAGNOSIS
PRIMARILY A CLINICAL DIAGNOSIS
LABORATORY INVESTIGATIONS
LABORATORY INVESTIGATIONS
 
Specific tests
Specific tests
Viral culture (gold standard)
Antigen detection – Immunofluorescence, Elisa
PCR
Serology
Non-specific tests –
Cytology --Giemsa stain (multinucleated giant cells )
                    --Papanicolaou stain - intranuclear  eosinophilic
    
           
 
inclusion bodies
 
Electron microscopy
 
INDICATIONS FOR ORAL ACYCLOVIR
INDICATIONS FOR ORAL ACYCLOVIR
 
Oral Acyclovir
Oral Acyclovir
Linear endothelitis
Diffuse 
endothelitis
Severe trabeculitis
Immunocompromised patients
Paediatric patients refractory to topical
Prophylaxis for post-PKP with h/o HSV
Prophylaxis against recurrent IEK
 
PROPHYLAXIS AGAINST RECURRENCE
PROPHYLAXIS AGAINST RECURRENCE
 
::Frequent  recurrent infection if b/l or involving an only
eye
::Post –PK patients with history of HSV keratitis
Tab acyclovir       400 mg   BD        * 12- 18 months
Tab famcyclovir  250 mg   OD       * 12 -18 months
 Valacyclovir        500mg   OD
       
* 12 - 18 months
     (for immunocompromised pt)
 
VARICELLA ZOSTER VIRUS
 
Incidence & epidemiology:
I.
Spread by saliva droplets, or direct contact with
infected rash.
II.
The maculopapular rash appears in successive crops,
lesions of various stages present simultaneously.
III.
Contagious period approx 1 day before rash &
continues approx 1 week after app of each crop of
lesion or until the cutaneous sores crust over.
IV.
IP: 12- 17 days after contact.
 
CLINICAL DISEASE
 
Congenital varicella syndrome
If mother contracts varicella during first or second
trimester of pregnancy.
Ocular findings ~ 
chorioretinits, optic nerve
atrophy or hypoplasia, congenital cataract 
and
Horner Syndrome.
No specific treatment.
Vaccinate all women with no history of previous
varicella.
 
 
HZO
 
First described by
Hutchinson in 1865
MC involves ophthalmic
division of 5
th
 nerve
Frontal branch is MC
involved
Nasociliary involvement
– 76% ocular involvement
 
Hutchinson’s sign –
vesicles at the side & tip
of nose precedes HZO
 
HZO lies dormant in TG
 
 
Herpes zoster keratitis
 
  Develops in about 50% within
   2 days of rash
 
  Small, fine, dendritic or stellate
   epithelial lesions
 
  Tapered ends without bulbs
 
  Resolves within a few days
 
  Develops in about 30% within
   10 days of rash
 
  Multiple, fine, granular deposits
   just beneath Bowman membrane
 
  Halo of stromal haze
 
Nummular keratitis
 
Acute epithelial keratitis
 
  May become chronic
 
OPHTHALMIC
COMPLICATIONS
 
 
Ramsay Hunt syndrome –
 
7
th
 nerve palsy + loss of taste
over ant 2/3
rd
 tongue +
earpain + vesicles in external
auditory canal or pinna
 
 
 
DIAGNOSIS
 
Diagnosis based on acute or recent history of systemic
ds with ocular or periocular  involvement with vesicles.
 
INVESTIGATIONS- vesicular fluid for PCR, immunomicroscopy
 
 
TREATMENT
 
 
ACTIVE DISEASE
 
1.
Antivirals( treat for 7 days , starting within 72 hrs) Famcyciclovir 500mg PO
TDS
 
 Valacyclovir 1 g PO TDS
 
Acyclovir 800mg PO 5t/d
 
2.
Lesions of lid, conjunctiva or cornea ( dendritic or rarely geographical
keratitis) –  
topical AV 
(trifluridine applied 9t/d * 7-10 days) plus 
an topical
AB.
 
3.      Late onset immune stromal ds treated similar to stromal herpes infection.
 
4.     Pain prevention-
 
TCA’s( eg nortryptyline, desipramine) 25-75 mg PO * 3months
 
Nonnarcotic or short term narcotic analgesic .
 
5.      Immunocompromised patients with any zoster –
 
I.V Acyclovir 15 – 20 mg/kg/day
 
ADENOVIRUS
KERATOCONJUCTIVITIS
 
Medium-sized (90–100 nm),
 nonenveloped (without an outer lipid bilayer)
icosahedral viruses composed of a nucleocapsid and a
double-stranded linear DNA genome.
 
OCULAR MANIFESTATIONS
1.
Epidemic keratoconjunctivits
2.
Pharyngoconjunctival fever
3.
Nonspecific follicular conjunctivitis
4.
Chronic adenoviral keratoconjunctivitis
 
 
EPIDEMIC KERATOCONJUCTIVIS
 
Serotype AD 8, 19, & 37.
 Most serious adenoviral ocular illness
In young adults during the fall and winter months
U/L in 2/3
rd
 pt
IP 8 days
Sign and symptoms:
  
 Acute tearing, FBS, photophobia, followed by lid
and conjuctival edema and hyperemia, follicular and
papillary conjuctival response with or without hge or
membrane formation, & tender LN’s
 
PHARYNGOCONJUCTIVAL
FEVER
 
CHRONIC ADENOVIRAL
KERATOCONJUCTIVITIS
 
 Serotype Ad 3 and 7
 
Similar to EKC except that the
keratitis is usaully mild and
b/l, and subepithelial
infiltrates are less frequent
and more transient.
 
Serotype Ad 2,3,4 and 19.
 
Uncommon, often recognized
cause of  ant segment
inflammatory and scarring
ds.
 
DIAGNOSIS & TREATMENT
 
Cytologic scrappings - mixed lymphocytic and neutrophil
infiltrate and degenerated epithelial cells.
Giemsa staining may reveal early eosinophillic intranuclear
bodies.
 
Antivirals are ineffective , except cidofovir.
Topicals NSIAD’S : relief of inflammation. No effect onviral
replication or appearance of corneal infiltrates.
Cycloplegics as needed for iritis.
Topical antibiotic ointment to lubricate and protect the
cornea in presence of membranes.
Ice packs, antipyretics and dark glasses as needed.
 
 
Genus Acanthamoeba:-
a 
family of free-living,
ubiquitous cyst-forming
protozoans.
 
Life cycle:- 2 forms
Generally rare infection
characterized by
periodic outbreaks
 
 
 
ACANTHAMOEBA
 
Acanthamoeba keratitis
 
  Contact lens wearers at particular risk
  Symptoms worse than signs
 
Pain disproportionate to clinical signs in early presentation
 
 Small, patchy anterior
 stromal infiltrates
 
  Perineural infiltrates
 (radial keratoneuritis)
 
 Ulceration, ring abscess
 & small, satellite lesions
 
-
Medical therapy given for 135 days
-
Biguanides(
chlorhexidine or polyhexamethylenebiguanide
(0.02%) effective against both forms
 
  Stromal opacification
 
Treatment
 
CORNEAL
SCRAPINGS
 
Epithelial scrapings for
LM
H & E stain
Giemsa
PAS stain
CFW stain
Acridine orange
stain
 
CULTURE
Non-nutrient agar with
e.coli
 
Source
Text-Kanski, Parson’s, Samar Basak, Pradeep
Sharma
Photographs- above , Archives & Website
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Herpes viruses are common human pathogens causing both asymptomatic infection and active disease. Ocular herpes, typically caused by HSV-1, presents with symptoms like pain, photophobia, and blurred vision. Factors like UV rays, trauma, and stress can trigger reactivation. Recurrent infections often originate from the trigeminal ganglion, affecting the eye via the ophthalmic division of the fifth cranial nerve. Understanding the mechanisms of HSV action and pathogenesis can aid in diagnosing and managing viral keratitis effectively.

  • Ocular herpes virus
  • Pathogenesis
  • Mechanism of Action
  • Clinical features
  • HSV-1

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  1. Dr Sanjeev Kumar Mittal Professor & Head, Ophthalmology 13-02-2018

  2. HERPES VIRUS Are ubiquitous human pathogen capable of causing both asymptomatic infection and active disease Humans are natural reservoir of HSV 2 types HSV 1- oropharynx HSV 2 genital area Ocular disease typically caused by type 1 Causes primary infection in children and neonates MODE OF INFECTION: IP 3- 9 days HSV 1 close contact HSV 2 venereal birth canal

  3. MECHANISM OF ACTION HSV (epitheliotropic & cytolytic) binds to one or morecellular receptor heparin sulphate Virus fuses with cell membrane Enters the cell and nucleus where the transcription of viral DNA occurs protein

  4. TG is the most common source of recurrent HSV infection. Primary infection may subsequently reactivate by travelling via ophthalmic division of 5th CN to the eye.

  5. PATHOGENESIS Factors for reactivation UV rays Trauma Heat, abnormal body temperature Other infectious disease Emotional disease Menstrual stress Steroids, immunosuppresant, PGs

  6. CLINICAL FEATURES Suspicion of viral keratitis arises if there is Associated skin lesions, recurrences of these lesions Stress-induced recurrence Immuno compromised status History of contact Symptomatic eye (Pain ,Photophobia ,Blurred vision, Tearing ,Redness) with minimal conjunctival and corneal signs Superficial dendrites with loss of corneal sensation

  7. CLASSIFICATION OF OCULAR DISEASE 1.Congenital & Neonatal 2. Primary infection 3. Recurrent infection

  8. CONGENITAL AND NEONATAL OCULAR HERPES May be acquired by one of the three periods : Intrauterine (5%) Peripartum(10%) Postpartum (85%) Intrauterine infection occurs in 1/300,000 births, with features of microophthalmia, retinal dysplasia, optic atrophy and chorioretinitis. HSV infections in latter two periods are further classified as skin, eyes, or mouth (SEM) with or without the other involvement seen in intrauterine infections. Ocular herpes include one or all: conjunctivitis, epithelial keratitis, stromal immune reaction, cataract, necrotizing chrioretinitis.

  9. PRIMARY INFECTION After 6 months maternal anti-HSV IgG Cutaneous involvement vesicular periocular skin eruptions , vesicular ulcerative blepharitis Acute follicular conjunctivitis Keratoconjuctivitis with non-suppurative lymphadenopathy Diffuse punctate keratitis that evolves into multiple scattered micro dendrite figures. As a rule confined to epithelium clinically d/t lack of previous immunologic stimulus Treatment-Topical antivirals supported by antibiotics & cycloplegics

  10. RECURRENT INFECTION Patients with recurrent herpes have both cellular and humoral immunity against the virus. corneal vesicles dendritic ulcer geographic ulcer(amoeboid) limbal ulcer (marginal)

  11. CLASSIFICATION OF HSV KERATITIS The disease may present as any one or a combination of the following: 1. Blepharoconjuctivitis 2. Episcleritis, scleritis 3. Infectious epithelial keratitis (IEK) 4. Neurotrophic keratopathy 5. Stromal keratitis Necrotizing stromal keratitis Immune (interstitial) keratitis Immune rings Limbal vasculitis Disciform keratitis 6. Endothelitis Disciform Diffuse Linear 7. Iridocyclitis 8. Trabeculitis

  12. Herpes simplex epithelial keratitis MC PRESENTATION Dendritic ulcer with terminal bulbs Stains with fluorescein May enlarge to become geographic In herpes, corneal sensation is reduced in approx 70 % of the patient. Aciclovir 3% ointment x 5 daily Ganciclovir ophthalmic gel 0.15% - 5 times daily Supported by antibiotics and cycloplegics Debridement if non-compliant Treatment 2-3wks

  13. D/D OF DENDRITIC KERATITIS Herpes zoster dendritic keratitis (pseudodendrites) Acanthamoeba keratitis Contact lens keratopathy Antiviral toxicity

  14. Herpes simplex disciform keratitis Signs Associations Central epithelial and stromal oedema Folds in Descemet membrane Small keratic precipitates - topical steroids (pred 1% or dexa 0.1%)+ with antiviral cover Treatment Occasionally surrounded by Wessely ring

  15. COTND. Oral (in immunodeficient or children) :: Acyclovir 400 mg PO 5t/d * 14 days, or ::Famcyclovir 500 mg PO twice daily for 14 days, or :: Valacyclovir 500 mg PO twice daily for 14 days, or

  16. Neurotrophic keratopathy ( Metaherpetic) Neurotrophic keratopathy. Damage to gasserian ganglion Impaired corneal innervations Decreased tear secretion Excess use of antivirals Signs Irregular cornea with loss of corneal lustre Characterized by persistent epithelial defect Oval in shape with gray, thickened smooth borders Rx-Stop all unnecessary medications Gentle debridement of boggy epithelium Artificial tears Mild steroid :If active stromal keratitis +ve Therapeutic soft CL Doxycycline 100mg PO once daily to inhibit collagenase Cycloplegics: if iritis is +ve Tarsorrhaphy to treat chronic exposure Cyanoacrylate glue if perforation occurs

  17. PRIMARILY A CLINICAL DIAGNOSIS LABORATORY INVESTIGATIONS Specific tests Viral culture (gold standard) Antigen detection Immunofluorescence, Elisa PCR Serology Non-specific tests Cytology --Giemsa stain (multinucleated giant cells ) --Papanicolaou stain - intranuclear eosinophilic inclusion bodies Electron microscopy

  18. INDICATIONS FOR ORAL ACYCLOVIR Oral Acyclovir Linear endothelitis Diffuse endothelitis Severe trabeculitis Immunocompromised patients Paediatric patients refractory to topical Prophylaxis for post-PKP with h/o HSV Prophylaxis against recurrent IEK

  19. PROPHYLAXIS AGAINST RECURRENCE ::Frequent recurrent infection if b/l or involving an only eye ::Post PK patients with history of HSV keratitis Tab acyclovir 400 mg BD * 12- 18 months Tab famcyclovir 250 mg OD * 12 -18 months Valacyclovir 500mg OD * 12 - 18 months (for immunocompromised pt)

  20. VARICELLA ZOSTER VIRUS Incidence & epidemiology: Spread by saliva droplets, or direct contact with infected rash. II. The maculopapular rash appears in successive crops, lesions of various stages present simultaneously. III. Contagious period approx 1 day before rash & continues approx 1 week after app of each crop of lesion or until the cutaneous sores crust over. IV. IP: 12- 17 days after contact. I.

  21. CLINICAL DISEASE Congenital varicella syndrome If mother contracts varicella during first or second trimester of pregnancy. Ocular findings ~ chorioretinits, optic nerve atrophy or hypoplasia, congenital cataract and Horner Syndrome. No specific treatment. Vaccinate all women with no history of previous varicella.

  22. HZO First described by Hutchinson in 1865 MC involves ophthalmic division of 5th nerve Frontal branch is MC involved Nasociliary involvement 76% ocular involvement Hutchinson s sign vesicles at the side & tip of nose precedes HZO HZO lies dormant in TG

  23. Herpes zoster keratitis Acute epithelial keratitis Nummular keratitis Develops in about 50% within 2 days of rash Small, fine, dendritic or stellate epithelial lesions Tapered ends without bulbs Resolves within a few days Develops in about 30% within 10 days of rash Multiple, fine, granular deposits just beneath Bowman membrane Halo of stromal haze May become chronic

  24. OPHTHALMIC COMPLICATIONS Ramsay Hunt syndrome 7th nerve palsy + loss of taste over ant 2/3rd tongue + earpain + vesicles in external auditory canal or pinna

  25. DIAGNOSIS Diagnosis based on acute or recent history of systemic ds with ocular or periocular involvement with vesicles. INVESTIGATIONS- vesicular fluid for PCR, immunomicroscopy

  26. TREATMENT ACTIVE DISEASE Antivirals( treat for 7 days , starting within 72 hrs) Famcyciclovir 500mg PO TDS Valacyclovir 1 g PO TDS Acyclovir 800mg PO 5t/d 1. Lesions of lid, conjunctiva or cornea ( dendritic or rarely geographical keratitis) topical AV (trifluridine applied 9t/d * 7-10 days) plus an topical AB. 2. 3. Late onset immune stromal ds treated similar to stromal herpes infection. 4. Pain prevention- TCA s( eg nortryptyline, desipramine) 25-75 mg PO * 3months Nonnarcotic or short term narcotic analgesic . 5. Immunocompromised patients with any zoster I.V Acyclovir 15 20 mg/kg/day

  27. ADENOVIRUS KERATOCONJUCTIVITIS Medium-sized (90 100 nm), nonenveloped (without an outer lipid bilayer) icosahedral viruses composed of a nucleocapsid and a double-stranded linear DNA genome. OCULAR MANIFESTATIONS 1. Epidemic keratoconjunctivits 2. Pharyngoconjunctival fever 3. Nonspecific follicular conjunctivitis 4. Chronic adenoviral keratoconjunctivitis

  28. EPIDEMIC KERATOCONJUCTIVIS Serotype AD 8, 19, & 37. Most serious adenoviral ocular illness In young adults during the fall and winter months U/L in 2/3rd pt IP 8 days Sign and symptoms: Acute tearing, FBS, photophobia, followed by lid and conjuctival edema and hyperemia, follicular and papillary conjuctival response with or without hge or membrane formation, & tender LN s

  29. CHRONIC ADENOVIRAL KERATOCONJUCTIVITIS PHARYNGOCONJUCTIVAL FEVER Serotype Ad 3 and 7 Serotype Ad 2,3,4 and 19. Similar to EKC except that the keratitis is usaully mild and b/l, and subepithelial infiltrates are less frequent and more transient. Uncommon, often recognized cause of ant segment inflammatory and scarring ds.

  30. DIAGNOSIS & TREATMENT Cytologic scrappings - mixed lymphocytic and neutrophil infiltrate and degenerated epithelial cells. Giemsa staining may reveal early eosinophillic intranuclear bodies. Antivirals are ineffective , except cidofovir. Topicals NSIAD S : relief of inflammation. No effect onviral replication or appearance of corneal infiltrates. Cycloplegics as needed for iritis. Topical antibiotic ointment to lubricate and protect the cornea in presence of membranes. Ice packs, antipyretics and dark glasses as needed.

  31. ACANTHAMOEBA Genus Acanthamoeba:- a family of free-living, ubiquitous cyst-forming protozoans. Life cycle:- 2 forms Generally rare infection characterized by periodic outbreaks

  32. Acanthamoeba keratitis Contact lens wearers at particular risk Symptoms worse than signs Pain disproportionate to clinical signs in early presentation CORNEAL SCRAPINGS Epithelial scrapings for LM H & E stain Giemsa PAS stain CFW stain Acridine orange stain Perineural infiltrates (radial keratoneuritis) Small, patchy anterior stromal infiltrates CULTURE Non-nutrient agar with e.coli Ulceration, ring abscess & small, satellite lesions -Medical therapy given for 135 days -Biguanides(chlorhexidine or polyhexamethylenebiguanide (0.02%) effective against both forms Stromal opacification Treatment

  33. Source Text-Kanski, Parson s, Samar Basak, Pradeep Sharma Photographs- above , Archives & Website

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