VIRAL CONJUNCTIVITIS

1. DR . ARNAV SAROYA

2. Introduction:-
Common External Ocular infection.
In 90% cases,Adenovirus is the causative agent.
May be Sporadic,or occur in epidemics.
Clinical hallmark of most viral conjunctivitis is the
follicular reaction of the conjunctiva, although this
feature may also be present in chlamydial infection
and toxic conjunctivitis as well.

3. CAUSATIVE AGENTS
• Adenovirusconjunctivitis(>90% cases).
• Herpessimplex keratoconjunctivitis.
• Herpeszoster conjunctivitis.
• Picorna viruses(Enterovirus and coxsackievirus).
• Poxvirusconjunctivitis.
• Myxovirus conjunctivitis.
• Parammyxovirus conjunctivitis.

4. Symptoms:-
• Watering
• Redness
• Irritation
• Itching.
• Photophobia(When Cornea is
involved).

5. Signs (Anterior to posterior):-
Eyelids :
edema,Ranging from mild to
Severe.
Lymphadenopathy:
Common. Tender Pre-auricular
nodes.
Conjunctiva:
Hyperemia, Follicles.
May be

6. PAPILLARY CONJUNCTIVITS
FOLLICULAR CONJUNCTIVITIS

7. Keratitis(Adenoviral):
Epithelial microcysts in the early stage.
Punctate epithelial keratitis. Usually occur in 7-10 days
of onset of symptoms. Resolving in 2 weeks.
Anterior Stromal infiltrates and subepithelial infiltrates,
may persist for months or years.
EPITHELIAL
MICROCYSTS
PUNCTATE EPITHELIAL
KERATITIS
SUBEPITHELIAL
INFILTRATES

8. Anterior uveitis:
Usually mild.
Severe Inflammation:
may be associated with conjunctival hemorrhages, chemosis,
membranes(Rare) and pseudomembranes.
Sometimes conjunctival Scarring.

11. Algorithm for Follicles:-
Follicles
Preauricular lymph nodes
Look for herpetic signs(e.g. dendrites,skin lesion)
Yes No
Source:Wills Eye Manual.
Yes No
HSV Adenovirus
Chlamydia
Toxic Conj.
Molluscum

12. ADENOVIRAL
CONJUNCTIVITIS
Non-enveloped, double stranded DNA viruses,
which replicatewithin the nucleus of hostcells.
General reservoir is onlyhuman.

13. Typeof adenoviralconjunctivitis
• Epidemic keratoconjunctivitis (EKC)
• Nonspecific acute follicular conjunctivitis
• Pharyngoconjunctival fever (PCF)
• Chronic /relapsing adenoviral
conjunctivitis

14. Spread of infection:-
Facilitated by
i)Virus can survive on dry surfaces for weeks.
ii)Viral shedding may occur for many days
before clinical features are apparent.
Transmission by
i)Contact with Respiratory or ocular
secretions. ii)Via Contaminated Fomites
such as Towels. iii)Route of transmission is
usually Eye-Hands-Eyes.

15. I)EPIDEMIC KERATOCONJUNCTIVITIS (EKC)
• Most severepresentation.
• Causedby adenoviruses type 8,19 and
37.It is markedly contagious.
• Incubation period after infection (8 days) &
virus shed from the inflamed eye for 2-3
weeks.
• Keratitis occurs in 80% cases.

16. •Pseudomembranes (inflammatory debris
and fibrin) or true membranes are a
marker of severe conjunctival
involvement.
•True membranes bleed when removed,
and their presence makes the patient
uncomfortable.
•Membranes can also rub against the
cornea, causing mechanical, geographic
ulcers that can mimic herpetic keratitis.

17. Membrane in a patient with epidemic keratoconjunctivitis (first
week). Detail, removal with forceps.

18. Follicles in a patient with
adenoviral infection. Fluorescein
demarcates the elevated follicles.
Epidemic keratoconjunctivitis.
Lid edema, crusting of the
eyelashes, and membrane

19. STAGES OF ADENOVIRAL KERATITIS
•Stage 1 usually occurs within the first week
after development of the adenoviral
conjunctivitis, with symptoms of worsening
discomfort, photophobia and lacrimation. This
is due to diffuse superficial epithelial punctate
keratitis caused directly by the live virus.
•Stage 2 is characterised by larger, fluorescein-
staining white punctate epithelial lesions, and
follows soon after Stage 1.
•Stage 3 occurs after a further 24-48 hours with
areas of combined epithelial and subepithelial
lesions.

20. •Stage 4 – the adenoviral conjunctivitis has usually
started to resolve, and the patient is left with non-staining
subepithelial lesions .
Stages 2–4 are thought to develop due to a delayed-type
hypersensitivity reaction to the epithelial viral antigens.
The adenoviral conjunctivitis usually resolves by two to
three weeks after onset, whereas Stage 4 keratitis
reaches its peak between week three and four.

21. TREATMENT
Supportive treatment for amelioration of
symptoms is the only treatment required and
includes:
I)Artificial tears 4x/d.Preferably
preservative free.
II)Cold Compresses
III)Discontinuation of contact lens wear.

22. IV)Removal of membranes/pseudomembranes.
V)Topical antibiotics.
VI)Povidone-Iodine:kills free adenoviruses.
VII)Topical Steroids:For severe Membranous or
Pseudo-membranous conjunctivitis and SEIs.
Corticosteroids enhance viral replication and increase
the duration of viral shedding.
VII) Zalcitabine, stavudine, and stampidineare
nucleoside reverse transcriptase inhibitors with different
degrees of anti-Ad activity.
IX)Topical Anti Histamines and vasoconstrictors.

23. II)NON-SPECIFIC ACUTE FOLLICULAR CONJ.
Most common form of acute follicularconjunctivitis
Causedby adenovirus serotypes 1 to 11 &19
Milder form of acute follicularconjunctivitis.
Unilateral symptoms, Other eyeinvolved 1-2 days
later, but less severely.
Patient may have systemic symptomssuch as
sore throat or commoncold.

24. NON-SPECIFIC ACUTE FOLLICULAR CONJ.

25. • Milder,andkeratitis is limitedto the epitheliumor
most commonly is notpresent.
• Ocular signs- limitedto amildFollicularreaction,
mildconjunctivalhyperemia,anddiscrete lid
edema.
• Preauricularadenopathymay bepresent.
• The identificationof these patients isimportant,
becausethey might notseek medicalassistance,
anddespitethe benignpresentationthey can
serve as a virus reservoir, spreadinga notalways
benigndiseaseinthe community.

26. III)PHARYNGOCONJUNCTIVA
L FEVER
• adenoviral infection commonly associated
with
subtypes3,4 & 7.
• Acute follicular conjunctivitis, associated with
pharyngitis.
• Fever& pre-auricular lymphadenopathy.
• Cornea :superficial punctate keratitis. (30%)

27. • Transmissible by three routes:
personal contact, fomites, or through
swimming pools or ponds.
•PCF is one of the most common illnesses seen
by
physicians at children’s summer camps
•PCF is most commonly bilateral, and the eyes
may be affected simultaneously or in sequence
up to 3
days apart.
•Hyperemia involves the entire conjunctiva but is
more prominent in the inferior fornix.

28. Child with features of PCF

29. Rare
Gives a clinical picture of chronic non-
specific follicles/papillaes.
Can persist over years, but eventually self
limiting
•The historical gold standard for adenovirus
conjunctivitis is cell culture with confirmatory
immunofluorescence staining (CC-IFA).

30. The symptoms persist longer than
expected for typical cases of
adenoviral disease, and the virus can
be recovered many months or years
after the onset of symptoms.
Conjunctivitis presents with
intermittent bouts of ocular irritation
with a waxing and waning superficial
punctate epithelial keratitis and with
SEIs

31. CHRONIC ADENOVIRAL CONJUNCTIVITIS

32. HERPES SIMPLEX VIRUS:-
Causes Follicular conjunctivitis
particularly in primary disease.
Usually unilateral.
Often Associated skin lesions.
Minute,Micro dendrites may be
mistaken for punctate epithelial
keratitis,But Corneal sensation is
reduced in HSV .

33. •Clinical course of the conjunctivitis is usually
limited to 2 weeks. Initial signs are similar to
adenovirus conjunctivitis, but the majority of the
patients will present unilateral disease. Mucous
discharge, conjunctival hyperemia, follicular
reaction, and enlarged preauricular nodes are
usually present at the first visit.
• Membranes and dendritic or dendrogeographic
conjunctival ulcers are uncommon findings.

34. •SYMPTOMS -itching, foreign body sensation,
and lacrimation.
•Clinical features - different from those in severe
cases of conjunctivitis caused by subgenera D
(Ad8, Ad19, and Ad37), which are associated
with pseudomembrane/membrane and SEIs.
However, HSV conjunctivitis presents features
similar to those caused by subgenera B
serotypes (Ad3, Ad7, and Ad11) but with a
shorter duration and a lower rate of bilateral
illness.

35. •Corneal involvement, such as typical dendritic
keratitis, may be present at the first visit or develop
later, especially in the immunocompromised patient
or in those treated with corticosteroids.
•Superficial punctate keratitis may be detected in
patients without dendritic lesions.
•Cell cultures are the gold standard method for
detecting HSV.
•Treatment of HSV conjunctivitis in the neonate is
mandatory and should include both topical antiviral
and intravenous acyclovir.

36. • HERPES SIMPLEX KERATITIS VESICLES IN HSV

37. VARICELLA ZOSTER VIRUS
•Highly contagious disease is characterized by a
mucocutaneous exanthem. Typically, lesions in
various stages are present simultaneously. The
infectious period ends only when all Lesions are
crusted.
•The conjunctiva is rarely involved. Small, ulcerative,
phlyctenule-like lesions at the limbus are the most
common finding.
•When the cornea is not affected, the patient can be
either carefully observed without treatment or
treated with topical antiviral ointments (3%
vidarabine or 3% acyclovir, 10–14 days).

38. •If keratitis is detected, treatment is
recommended.
•VZV gains access to the sensory ganglia during
the primary disease (varicella).
The reactivation of latent virus in the trigeminal
ganglion leads to the involvement of V1
(ophthalmic nerve) dermatome and is referred to
as herpes zoster ophthalmicus.

39. VZV KERATITIS

40. ACUTE HEMORRHAGIC CONJUNCTIVITIS:-
• Usually occurs in tropical areas.
• Caused by Enterovirus and coxsackie
virus(Picorna virus family).
• Rapid onset,resolves within 1-2weeks.
• Enterovirus type 70 (EV70) and coxsackievirus
A type 24 variant (CA24v) (picornavirus family)
are the most common causes of acute
hemorrhagic conjunctivitis (AHC)

41. • Although EKC with
prominent
subconjunctival
hemorrhages may
resemble AHC, the latter
has a shorter incubation
time, a more rapid
disease course, and less
corneal involvement.
• TREATMENT-
• cold compress, artificial
tears) and contagion
• precautions should be
prescribed.

42. PARAMYXOVIRUSES
•Family includes the viruses of measles,
Newcastle disease, and mumps.
•Measles is a highly contagious viral
infection.
•Transmission- via large respiratory
droplets.
•The clinical features are high fever,
cough, runny nose, and a generalized
maculopapular rash.

43. •Catarrhal conjunctivitis, superficial
keratitis, and photophobia are the
most common clinical features in
healthy individuals.
•Subconjunctival hemorrhages may be
present.
•Keratitis is usually severe in patients
with vitamin A deficiency.

44. •Newcastle disease -limited to poultry workers and
laboratory personnel.
•Infection is usually acquired when dealing with
infected poultry or directly with infected material.
• Ocular disease is characterized by mild follicular
conjunctivitis and tearing.
•Subepithelial infiltrates might be present.
Mumps -acute viral infection characterized by swelling
(more commonly bilateral) of the parotid salivary
glands.
•Orbital pain and a mass are present when the
lacrimal gland is affected.
•Superficial punctate keratitis or stromal keratitis may

45. MOLLUSCUM CONTAGIOSUM:-
Caused by dsDNA pox virus.
Peak incidence of getting the virus is 2-4years.
Typically,Virus causes a skin lesion.
When skin lesion is on the lash line area of eyelid,it
causes viral shedding and follicular conjunctivitis.
Examine eyelash line carefully when Chronic,unilateral
eye irritation and mild discharge is present.
The typical presentation of ocular involvement is a
follicular conjunctivitis and lid margin lesions. MC
lesions are often raised, umbilicated, waxy, and flesh
coloured

46. Molluscum eyelid lesion:

47. TREATMENT -
•Surgical removal (simple excision, curettage)
of the lesions is curative in most cases.
•Cryotherapy is effective, but depigmentation
of the treated area is a risk.
•AIDS patients may present with exuberant
and/or recalcitrant MC.
•Meticulous surgical removal, electron beam
radiation, carbon dioxide laser, and topical
cidofovir can be effective in these patients.
Remission can also be observed with
administration of highly active antiretroviral
therapy.

48. Investigations:-
Giemsa stain.
PCR
Viral culture.
Immunochromatography.
Serology.
For other causes in non-resolving
cases.

49. Reduction of Transmission Risk:-
Meticulous hand hygiene.
Avoiding eye rubbing and towel
sharing.
Disinfection of instruments and
clinical surfaces after examining an
infected person.

50. REFERENCES:-
Krachmer
Kanski
Peyman’s
Copeland and Ashrafi’s principles and
practice of cornea