uvea

1. INFECTIVE UVEITIS

2. INTRODUCTION
 The etiology of uveitis is complicated and includes
infectious,noninfectious and neoplastic causes.
 It is useful in clinical practice to rule out infectious causes
first and to consider the most common infectious etiologies
at the onset.
 There is a long list of possible systemic infections which can
cause uveitis.
 It is essential for the ophthalmologist to take a
comprehensive history and review of systems to obtain any
diagnostic clues related to possible infection.
2

3. International uveitis study group (IUSG) proposed clinical
classification of uveitis:-
Infectious NON INFECTIOUS MASQUERADE
1.Bacteria
2.Viral
3.Fungal
4.Parasitic
5.Others
1.Knownsystemic
association
2.Noknown systemic
Association
1.Neoplastic
2.Non neoplastic
3

4. INFECTIVE UVEITIS
Bacterial causes :- Viral causes:-
1. Tuberculosis 1.Cytomegalo virus
2. Syphilis 2.Herpes simples
3. Leptospirosis 3.Herpes zoster
4. Brucellosis 4.Chikungunya
5. Leprosy 5.Westnile virus
4

5.  Fungal causes:-
1.Nocardia
2.Candidiasis
3.Histoplasmosis
4.Cryptococcus neoformans
5.Aspergillosis
 Parasitic causes:-
1.Toxoplasmosis
2.Toxocaracanis
3.Cysticercosis
4.Onchocerca volvulus
5

6. TUBERCULOSIS
 It is mainly a pulmonary disease but intraocular tuberculosis(IOTB)
is a rare form of extrapulmonary TB.
 It occurs as a consequence of primary infection,dissemination of
systemic infection, reactivation of latent TB,or immune mediated
disease.
 Anterior uveitis is the most common manifestation and is is usually
granulomatous.
6

7. PATIENTS WHO SHOULD BE INVESTIGATED FOR OCULAR TB
Presumptive ocular TB :-A patient with one of the following
clinical presentations:
 Granulomatous anterior uveitis
 Non-granulomatous anterior uveitis, not associated with any
other known clinical entity, e.g. HLA-B27
 Intermediate uveitis, with/without healed/active focal lesions
 Posterior uveitis, including subretinal abscess, choroidal/disc granuloma,
multifocal choroiditis, retinal periphlebitis and multifocal serpiginous
choroiditis.
 Panuveitis.
 Rarely, scleritis (anterior and posterior), interstitial and disciform keratitis
 Note: Extraocular TB disease is often absent in ocular TB patients,and
patients do not usually have systemic symptoms of fever and weight loss.
7

8.  Anterior tuberculous uveitis:-
 Usually granulomatous.
 Muttonfat keratic precipitates.
 Broad based synechiae.
 Iris nodules(less frequent)
 Intermediate uveitis:-
 Vitreitis
 Snow balls
 Phlebitis with cystoid macular edema
8

9. ANTERIOR UVEITIS
9

10. INTERMEDIATE UVEITIS
10

11.  Posterior uveitis:-
 Choroiditis :- charachterised by deep,yellow,multiple lesions usually
diagnostic of disseminated TB. Multifocal serpiginoid choroiditis is
specific for tuberculous uveitis
 Choroidal tubercles:-
Small (approx 0.3-3.0mm) yellow nodules with indistinct borders that
may become pigmented as they heal and scar.
11

12.  Choroidal granuloma:-
A very large abscess like tubercle is known as Tuberculoma. These
are larger usually more than two disc diameters,solitary,tumour
like masses that may grow vertically or spread diffusely in the
choroid.
12

13.  Retinal vasculitis:-
 Is preferentially venous.
 Retinal hemorrhages are common.
 Some cases of Eales ‘disease represent hypersensitivity to TB.
 Other manifestations:-
 Reddish brown eyelid nodules(lupus vulgaris).
 Conjunctivitis.
 Phlyctenulosis.
 Interstitial keratitis.
 Scleritis.
 Exudative retinal detachment.
 Optic neuritis,neuroretinitis,papillitis.
13

14. Classification of IOTB:-
Clinical diagnostic group
1.Confirmed IOTB:-(both 1 and 2)
 Atleast one clinical sign suggestive of IOTB.
 Microbiological confirmation of MTB from ocular fluids/tissues.
2.Probable IOTB( Both1,2,3):-
 Atleast one clinical sign suggestive of IOTB(and other etiologies
excluded).
 Evidence from chest X-ray,clinical evidence of extra
ocularTB,microbiological confirmation from sputum or extraocular
sites.
 Atleast one of the following:-
a) Documental exposure to TB
b) Immunological evidence of TB infection.
14

15. 3.Possible IOTB(1,2,3 together) or(1 and 4):-
 Atleast one clinical sign suggestive of IOTB(and other
etiologies excluded).
 Chest X-ray not consistent with TB infection and no clinical
evidence of extra ocularTB.
 Atleast one of the following:-
a) Documental exposure to TB
b) Immunological evidence of TB infection.
 Evidence from chest X-ray,clinical evidence of extra
ocularTB,microbiological confirmation of extra ocularTB,but
none of the charachteristics consistent GIVEN IN 3.
15

16. INVESTIGATIONS:-
 Systemic assessment by-
 Sputum testing with PCR
 Interferon gamma assay
 Chest x-ray
 HIV test
 PET/CT
 Aqueous/vitreous sampling rarely yields demonstrablemycobacteria
 OCT- for macular evaluation.
 FFA- for demonstrating ischemia in active choroiditis.
 Histopathological evidence of TB- GOLD STANDARD.
16

17.  TREATMENT:-
 ANTI-TB multidrug therapy.
 Topical and systemic steroids.
 Laser –applied to ischemic retina to treat preretinal
neovascularisation.
17

18. RESPONSE TO TREATMENT:-
Treatment success or failure is primarily guided by the
level of inflammation seen inside the eye.
 Remission: Inactive disease for at least 3 months after
discontinuing all therapy.
 Treatment failure: No decrease in inflammation, or less
than a two-step decrease in level of inflammation after
3 months of ATT (inflammatory scores of fundus lesions
such as retinal perivasculitis or multifocal serpiginous
choroiditis are not yet defined and are left to the
judgment of treating physicians).
 Relapse: An increase in the level of inflammation after
complete remission (at least two-step increase).
18

19. The main indications for surgery in ocular TB are as
follows:
 Complications of retinal vasculitis—retinal
neovascularization, vitreous haemorrhage, tractional or
combined retinal detachment, epiretinal membrane.
 Diagnostic vitrectomy when conventional methods fail
to establish diagnosis.
 Non-resolving vitreous inflammation.
 Visually significant vitreous floaters after completion of
medical therapy.
 Management of complications of uveitis such as
cataract and glaucoma.
19

20. SYPHILITIC UVEITIS
 Caused by spirochete bacterium Treponema pallidum.
 Mode of transmission:-
 Sexual transmission
 Parenteral transmision
 Transplacental infection of fetus.
 Spirochetes can rapidly penetrate mucous membranes or
small skin abrasions and migrate to lymphatics.
 Because the clinical presentation of ocular syphilis is so
varied, ocular syphilis has been classically regarded as ‘‘the
great imitator.’’
20

21.  Syphilis has 3 clinical stages:-
1. Primary syphilis - painless chancre
2. Secondary syphilis – fever,malaise, mucocutaneous
lesions.Most infectious stage with highest systemic load.
3. Tertiary syphilis - gummas and involve vasa vasorum of
aorta and CNS.
21

22. CLINICAL FEATURES :-
 Anterior segment involvement:-
 Conjunctivitis
 Scleritis
 Interstitial keratitis
 Iridocyclitis
 Posterior segment involvement:-
 Vitritis
 Chorioretinitis
 Serous retinal detachment
 vasculitis
22

23. SYPHILITIC ANTERIOR UVEITIS
 Unilateral or bilateral
 Granulomatous or nongranulomatous
 Anterior with or without anterior vitreitis
 Interstitial keratitis
 Dilated iris vessels
(roseolae of iris)
 Lens dislocation
 Iris atrophy
23

24. SYPHYLITIC POSTERIOR UVEITIS
 The most common posterior segment presentation
is CHORIORETINITIS.
 Associated with secondary stage of disease.
 4 types of presentation:-
 Diffuse choroiditis
 Disseminated syphilitic chorioretinitis
 Peripheral /anterior choroiditis
 Localised syphilitic choroiditis
24

25. DIFFUSE CHOROIDITIS
 Occurs as early infection.
 Disappears on treatment.
 Leaves no trace except fleck form areas of superficial
choroidal atrophy.
25

26. DISSEMINATED SYPHILITIC CHORIORETINITIS
 Most common manifestation of chorioretinal syphilis.
 Occurs in late secondary stage.
 Bilateral usually.
 Symptoms:-metamorphopsia,photopsia
 Signs- 1.cloud of vitreous opacities
2.greyish yellow areas of acuteinflammation
3.Retinal edema and blurring of disc.
26

27. 27

28.  Cases of ocular syphilis should be investigated for
concomitant HIV infection.
TREATMENT:-
 Aqueous penicillinG (2-5 milion units IV every 4 hours
for 10-14 days).
PROGNOSIS :-
 In secondary stage-prognosis is good though iritis is
present.
 In tertiary stage prognosis is bad due to development of
glaucoma.
 50% develop visual impairement
 10% eventually become blind 28

29. BRUCELLOSIS
 MC zoonotic disease world wide.
 Caused by gram negative bacteria Brucella melitensis or
Brucella abortus.
 It is transmitted from animals to man through ingestion
of unpasteurised milk products or uncooked meat.
 Ocular manifestations:-
 Uveitis after acute phase –it may be chronic anterior
uveitis or multifocal choroiditis.(MC)
 Panuveitis is reported in 1/5th of all cases. in 1/5tf
 Dacryoadenitis
 Epi Scleritis
29

30.  Nummular keratitis
 Optic neuritis,optic neuropathy,papillitis.
 Papilledema
 Retinal detachment,retinal hemorrhages.
 Extraocular palsies.
DIAGNOSIS:-
 Standard agglutination test,ELISA
 IgM , IgG for brucella.
 Positive blood culture.
TREATMENT :-
 Tetracycline or doxycycline for 6 weeks.
 In case of eye involvement local and systemic corticosteroids for
2-4 weeks.
30

31. LYME DISEASE(BORRELIOSIS)
 It is an infection caused by a flagellated spirochaete
bacterium Borrelia burgdorferi .
 Transmitted through the bite of a hard-shelled tick of
the genus Ixodes.
 Systemically pathognomonic annular expanding skin
lesion at the site of bite - ‘Erythema Chronicum Migrans’
are seen.
31

32. Ocular Manifestations-
 In Early stage
 Conjunctivitis
 Episcleritis may be seen
 In Later stages
 Uveitis is seen which may be in the form of anterior
uveitis, intermediate uveitis.
 neuroretinitis,
 choroiditis and panuveitis.
 Severe vitritis is frequently present.
 If infection persists over a few months, keratitis
develops.
32

33. Diagnosis of Lyme borreliosis :-
 Is primarily based on clinical presentation with support from
laboratory data.
 IgM & IgG by ELISA or IFA .
Treatment of:-
 Acute disease involves oral doxycycline and streptomycin.
 Patients with advanced disease with ocular manifestations
should be started on intravenous ceftriaxone.
33

34. LEPROTIC UVEITIS
 Chronic granulomatous infection.
 caused by Mycobacterium leprae and M. lepromatosis.
 Mode of spread - nasal secretions.
 Predominantly involves anterior uvea.
34

35. Investigation:-
 Skin, and ocular specimens show acid-fast bacilli.
 The lepromin test distinguishes between tuberculoid
and lepromatous leprosy.
Treatment:-
 Systemic Combination regimens of extended duration
with antibiotics such as dapsone, rifampicin and
clofazimine.
 Ocular Anterior uveitis is treated with steroids.
35

36. PURULENT UVEITIS & ENDOPHTHALMITIS
Endophthalmitis usually presents with:
 Significant intraocular inflammation
 may be categorized as exogenous or endogenous.
 Purulent exogenous uveitis occurs in healthy patients –
- Generally seen after surgery,
- by contiguous spread from an external ocular
infection, or after trauma.
 Usually the vitreous is affected first & organisms grow readily in it,
Purulent cyclitis, retinitis and choroiditis develop.
Endogenous Endophthalmitis: -
Occurs primarily in patients :-
 who are relatively immunocompromised
 The most commonly encountered type of fungus is Candida albicans
36

37. In the exogenous form following changes occur-
 Edges of the wound become yellow and necrotic.
 A hypopyon appears .
 Vitreous becomes purulent (seen as a yellow fundus reflex).
 It may progress to Panophthalmitis in which there may be
 Proptosis ,
 painful limitation of movement (due to extension of
inflammation to the tenon’s capsule) .
 In sever cases:
 Formation of cyclitic membranes &
 Destruction of ciliary processes leading to a fall in IOP resulting
in shrinkage of the globe (pthisis bulbi).
37

38. DIAGNOSIS OF ENDOPHTHALMITIS
 Detailed history & examination .
 B-scan is required to confirm the clinical diagnosis by
demonstrating exudates in the vitreous.
 At first a conjunctival swab should be sent for Gram
staining & culture.
 Anterior chamber tap and Vitreous tap or biopsy
 After a vitreous tap, a single injection of antibiotics with
or without dexamethasone is given into the vitreous
cavity.
 Vancomycin (1mg) & Ceftazidime (2.25mg) are the
preferred combination for intravitreal injection.
38

39. BASED ON THE RESULTS OF THE ENDOPHTHALMITIS
VITRECTOMY STUDY GROUP
39

40. FUNGAL ENDOPHTHALMITIS
 Characterized by creamy white, well-circumscribed
chorioretinal lesions ,often in the posterior pole with
associated yellow or white fluffy vitreous opacities.
 Vitreous fungus balls sometimes coalesce to form the
classic ‘‘string of pearls’’ configuration.
40

41. VIRAL UVEITIS
 Viral uveitis is a spectrum of diseases predominantly of herpes
family of viruses.
(Varicella zoster,herpes simplex,cytomegalovirus, ebsteinbarr
virus)
 The clinical picture often depends on hosts immune status:-
 Acute retinal necrosis(ARN) is most often found in an
immunocompetent host.
 Progressive outer retinal necrosis and CMV retinitis are seen in
an immunocomprimised host.
41

42. HERPES SIMPLEX VIRUS
 It presents as anterior uveitis.
 Crops of vesicles seen.
 Keratic precipitates are fine,stellate and diffusely distributed
across the cornea.
 Patchy and occasionally sectoral iris atrophy that includes
pigment epithelium is common.
42

43. TREATMENT :-
 Topical steroid
Eg.prednisolone acetate 1% ,4 times daily and a topical
cycloplegic.
 Oral antiviral
Eg.Aciclovir 400mg 5 times/day or famciclovir or
valaciclovir.
 Steroids may be used with caution if epithelial defect is
present.
43

44. VARICELLA ZOSTER VIRUS
 Anterior uveitis:- Onset is 1-3 weeks after acute skin rash and
affects nearly 50% of patients with herpes zoster
ophthalmicus.
 Herpeszoster ophthalmicus without dermatitis known as
ZOSTER SINE HERPETE.
 Iridocyclitis may be recurrent.
 Granulomatous inflammation,sectoral iris atrophy present.
 Anterior segment inflammation can oocur in primary VZV
infection,particularly in immunocomprimised.
 Neuroretinitis is rare.
44

45. TREATMENT:-
 Topical steroids and mydriatics.
 Systemic steroids are required rarely.
 Persistence or reccurence of anterior uveitis may respond to
oral aciclovir 800mg 5times a day.
 VZV vaccination protects against shingles.
45

46. CMV RETINITIS
 Cytomegalo virus is a ds DNA in the herpesviridae family.
 Anterior uveitis is the hallmark of CMV infection in
immunocompetent individuals.
 Reactivation of CMV is seen in patients with CD4 count <50/mm3.
 CMV RETINITIS is categorised as:-
 Fulminant (Edematous):-
 Large areas of hemorrhage and a white,edematous or necrotic
retina .
(also known as PIZZA PIE APPEARNCE)
46

47.  Granular /atypical/indolent:-
Granulomatous lesion with small dot infiltrates without hemorrhages.
It may appear as scar lesion but continues to progress slowly.
 Perivascular form/frosted branch angitis:-
Diffuse vascular retinal sheathing,activeretinitis progressing from
borders of lesion sometimes with hemorrhage,papillitis.
47

48. Diagnosis:-
 Usually clinical.
 In atypical patients,PCR from vitreous or aqueous tap provides high
sensitivity or specifity.
Treatment:-
 Intravitreous injections of either ganciclovir or foscarnet (5mg/kg
ganciclovir twice daily for 2-3 weeks followed by 5 mg/kg/day as
maintanence.)
 A better alternative is Ganciclovir slow-release device(vitrasert)
and is as effective as intravitreous therapy.
 Duration of efficacy is 8 months which is superior to intravitreous
therapy.
 The implant is left suspended in the vitreous and sutured to sclera.
48

49. ACUTE RETINAL NECROSIS
 ARN is a rare but devastating necrotising retinitis.
 It typically affects the otherwise healthy individuals of all
ages.
 Males >females (2:1)
 ARN is a biphasic disease which tends to be caused by herpes
simplex virus in younger patients and varicella zoster virus in
older individuals.
 Presentation is usually unilateral and varies according to
severity.
49

50. 50

51.  The evolution of ARN starts with moderate to severe Viritis that
progress to involve peripheral, well delimited patches of retinal
necrosis.
 Without treatment,the lesions tend to rapidly progress in a
circumferential pattern in 5-10 days. Posterior pole is usually
spared until late.
 The acute lesions resolve within 6-12 weeks ,leaving behind
transparent necrotic retina with hyperpigmented borders.
 A sharp demarcation line forms between affected and normal
retina which is a high risk for retinal breaks and detachment
(50-75%).
 Unless the patient receives appropriate treatment bilateral disease
(BARN) occurs in upto 30-35% of cases within 6 weeks.
51

52. 52

53. TREATMENT:-
 Intravenous acyclovir (10mg/kg every 8 hrs) for 7 to 14 days
which is followed by:-
 Oral acyclovir 800mg 5times daily for 6-12 weeks -
Given to decrease the immediate risk to recurrence.
 In severe cases intravitreal ganciclovir or foscarnet may also
be used to enhance the prognosis.
 Systemic steroids may be started 24 hrs after initiation of
antiviral therapy to control inflammatory response.
 Laser retinopexy around necrotic areas-to prevent RRD .
 Vitrectomy for RRD, commonly with silicone oil tamponade.
53

54. PROGRESSIVE OUTER RETINAL NECROSIS(PRN/PORN)
 Occurs predominantly in AIDS.
 It may also occur in patients with drug induced
immunosuppression.
 The most common cause is Varicella zoster virus.
 PORN begins as multifocal patchy areas of outer retinal
whitening that coalesce rapidly.
 In contrast to ARN-
 The posterior pole is involved early in the course of disease.
 Vitreous inflammatory cells are typically absent.
 Retinal vasculature is minimally involved.
54

55. Retinitis- Three stages are recognized:
 Early:-macular involvement showing cherry red spot appearance.
 Established/middle:-Extensive full thickness necrosis of retina .
 Late. :-Scarring is plaque-like and characterized as ‘cracked mud’.
Rhegmatogenous retinal detachment (RRD) is very common.
55

56.  There is more outer retinal involvement.
 There is more rapid progression of lesions in PORN than in
ARN.
 Bilateral disease is reported in more than 70% of patients.
DIAGNOSIS:-
 Mainly clinical.
 Definitive diagnosis is made by specific PCR- based
diagnostic assay for VZV DNA Performed on vitreous
samples.
56

57. Treatment of progressive outer retinal necrosis involves:-
 Intravenous foscarnet and ganciclovir for 7-14 days.
 Intravitreal foscarnet and ganciclovir should be used 1-2 times
per week for 2 weeks.
 High risk for retinal detachment in upto 50%-75% of
patients,there is role of Prophylactic laser photocoagulation
that may reduce the risk for retinal detachment.
 Prophylactic laser photocoagulation should be applied in 3-4
rows at the posterior border of the advancing retinitis.
57

58. UVEITIS IN HUMAN IMMUNODEFICIENCY VIRUS INFECTION
Ocular features:-
 Eyelids:- Blepharitis, Kaposi sarcoma, multiple molluscum lesions
and herpes zoster ophthalmicus.
 Orbit.:-Cellulitis (e.g. aspergillosis, contiguous sinus infection), B-
cell lymphoma.
 Conjunctiva:- Kaposi sarcoma, squamous cell carcinoma and
microvasculopathy (up to 80%).
 Cornea.:-Keratoconjunctivitis sicca ,keratitis, e.g. herpes simplex ,
herpes zoster and fungal.
 Anterior uveitis commonly with drug toxicity, e.g. rifabutin,
cidofovir.
 HIV-related retinal microangiopathy.:-Retinal microangiopathy is the
most frequent retinopathy in patients with AIDS(70%).
58

59.  Other viral retinitis: cytomegalovirus retinitis (most common),
PRN,ARN.
 Protozoal: -toxoplasmic retinochoroiditis.
 Fungal: Pneumocystis choroiditis, Histoplasma chorioretinitis,
cryptococcal choroiditis, candidiasis.
 Bacterial: syphilis, tuberculosis.
 Neoplastic: B-cell intraocular lymphoma.
 Neuro-ophthalmological. Usually secondary due to an opportunistic
infection (e.g.toxoplasmosis, cryptococcosis, neurosyphilis) or
neoplastic process (e.g. CNS lymphoma)
59

60. FUNGAL UVEITIS
HISTOPLASMOSIS
 Histoplasma capsulatum infection occurs following
inhalation of yeast form of this dimorphic fungus and
can lead to systemic mycosis histoplasmosis.
 Pulmonary involvement is common.
 Eye disease represents an immune mediated response
to microbial antigen ,rather than due to active infection.
60

61. PRESUMED OCULAR HISTOPLASMOSIS SYNDROME -
(POHS)
An ocular syndrome with classical triad of-
 Multiple white atrophic chorioretinal histo spots about
200micro metres in diameter.
 Pigmented peripapillary degeneration
 Vitrietis is absent.
61

62.  60% have bilateral signs.
 POHS is asymptomatic unless it causes choroidal
neovascularisation (CNV).
 CNV is associated with an old macular ‘histo spot’ . Choroidal
neovascularization in the macula can cause a sudden, abrupt
decrease in the central vision.
INVESTIGATIONS:-
1. HLA testing:- HLA-B7 ,DRW2
2. Serological testing
3. FA and OCT when CNV is suspected.
62

63. TREATMENT:-
 If vision is threatened, the treatment approach is-
 Argon laser photocoagulation for extrafoveal CNV and
 Photodynamic therapy (PDT) for subfoveal membranes
is advocated.
 Intravitreal anti-VEGF drugs may be effective for both
extrafoveal and subfoveal CNV .
 Amsler grid testing for fellow eye atleast weekly,
particularly if histospot is present.
63

64. PNEUMOCYSTIS CHOROIDITIS
 Caused by PNEUMOCYSTIS JIROVECII.
 A pulmonary commensal.
 Seen in uncontrolled AIDS.
 OCULAR FEATURES:
 Multiple slowly progressive deep round,yellow orange lesions
are characheristic.
 Commonly bilateral.
 Minimal vitritis.
 Visual loss is negligible.
64

65. Treatment :-
 Systemic antimicrobial prophylaxis.
 Immune reconstitution .
Has dramatically reduced the incidence of pneumocystis
choroiditis.
65

66. CRYPTOCCOCAL CHOROIDITIS
Cryptococcus neoformans
(dimorphic yeast)
inhalation
Blood stream CNS
Eye Optic nerve
66

67.  Ocular features:
 Multifocal choroiditis - Direct involvement
 Vasculitis
 Papilloedema - Indirectly
 Ocular motilitydysfunction
67

68. ENDOGENOUS CANDIDA ENDOPHTHALMITIS
candida albicans(commensal)
EYE
Exogenously Endogenously
 Trauma 1. IV drug abuse
 Surgery 2. Septic focus –
 fungalkeratitis indwelling catheter
3.Cystic fibrosis
4.General debilitation
5. Diabetes
 Uncommon in AIDS. 68

69.  Ocular involvement is seen in 1/3rd patients with untreated
candidemia.
 Peripheral fundus lesions may cause little or no visual
disturbance.
 Central lesions or severe vitritis will manifest earlier.
 Vitritis may be marked with fluffy cotton ball or string of
pearls colonies.
 Chorioretinitis:- one or more small creamy white lesions with
overlying vitritis
 Retinal necrosis may lead to retinal detachment with severe
proliferative vitreoretinopathy.
69

70. 70

71. INVESTIGATIONS:-
 Vitreous biopsy(PCR,Culture)
 Systemic investigation:-blood and urine culture
Treatment :-
 Antifungal treatment:-
Acc to infectious diseases of america guidelines-
 Intravenous amphotericin –B in combination with oral flucytosine .
 Voriconazole intravenously or orally –has high ocular penetration
 Parsplana vitrectomy-reduces fungal and antigen load,facilitates
therapeutic agent penetration and clears ocular media.
71

72. ASPERGILLUS ENDOPHTHALMITIS
Aspergillus species
Airborne spread
Risk factors:-1. IV drug abuse
2.Chronic lung disease
3.Organ transplantation
4.Blood disorders(NEUTROPENIA)
OCULAR FEATURES:-
 Iridocyclitis and vitritis are common.
 Yellowish retinal and subretinal infiltrates tend towards macular
involvement.
72

73.  Occlusive retinal vasculitis is common.
 Visual outcome is worse.
 Investigations and treatment are similar to candida
endophthalmitis.
73

74. PARASITIC UVEITIS
TOXOPLASMOSIS
 Toxoplasma gondii is a single-cell, obligate, intracellular
protozoan and is likely the most common cause of infectious
posterior uveitis in the world.
 Cat - definitive host .
 Intermediate hosts include mice, livestock and humans .
 It is transmitted either by maternal transmission during
pregnancy (often in the third trimester) or by ingestion of
raw or undercooked meat with tissue cysts or from
contaminated fruit, vegetables, or water.
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76. CLINICAL FEATURES OF TOXOPLASMOSIS
CONGENITAL TOXOPLASMOSIS:
 Occurs because of transplacental transmission early in the
course of pregnancy.
 Retinochoroiditis is the most common manifestation of
congenital toxoplasmosis
 There are bilateral, multiple chorioretinal lesions in the fundus,
usually involving the macula.
 In these infants, the ocular lesions are usually associated with
encephalitis and there is history of convulsions.
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77.  The entire thickness of the retina and choroid is destroyed in a
necrotizing inflammation so that a punched-out, heavily
pigmented scar remains.
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78. ACQUIRED TOXOPLASMOSIS
 The classic lesion is a focal necrotizing retinochoroiditis
accompanied by vitreous inflammation.
 The acute lesion typically arises from the border of a
chorioretinal scar.
 These lesions often remain active for up to 16 weeks and then
resolve, leaving a hyperpigmented scar.
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80.  Toxoplasmosis in immunocompromised patients can be
multifocal and may also expand into large areas of full-
thickness retinal necrosis.
 These lesions are more resistant to treatment and have a
poorer prognosis.
 OCT findings in acute ocular toxoplasmosis may include :-
 Retinal thickening with macular edema.
 As the lesion heals, there is often significant retinal thinning
with excavation of the retinal and subretinal layers including
the choriocapillaries.
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81. DIAGNOSTIC TESTING FOR TOXOPLASMOSIS
 The definitive diagnosis of toxoplasmosis is made by direct
demonstration of the organism in tissues or bodily fluids by in
vitro culture or by polymerase chain reaction (PCR) .
 Serologic methods are the main tools for confirming exposure to
T. gondii in cases of suspected toxoplasmosis .
 Serological Testing:
 Sabin-Feldman dye test (titre greater than 1:16).
 Complement fixation test .
 Indirect Haemagglutination test .
 ELISA for IgG & IgM.
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82. TREATMENT :-
 The goal of treatment of toxoplasmosis is to stop the replication of
the organism and limit inflammation within the eye .
 SULPHA TRIAD:
 Sulphadiazine
 Sulphathiazole
 Sulphamerazine
 These 3 drugs in a dosage of 500mg tablets each are given every 6
hours along with pyrimethamine 75-100mg twice for 1-2 days
followed by 25-50mg daily thereafter, are continued for 4-6 weeks.
 Folinic acid (5mg 3times a week) is added to prevent bone marrow
suppression caused by pyrimethamine.
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83.  Alternatively, Clindamycin along with Sulphadiazine can be given:
Clindamycin oraly 300mg 6 hourly + Sulphadizine (Loading dose of
2gms followed by 1gm 6 hourly).
 Concomitant use of corticosteroids limits intraocular inflammation
should be considered within a few days of initiation of antibiotics.
 Prednisolone (1mg/kg) is given initially and tapered acc.to clinical
responsebut always in conjunction with anti-toxoplasma agent.
 Suitable alternative for patients who are intolerant of or unresponsive
to systemic medications:
Intravitreal clindamycin (1.0- 1.5 mg/0.1 ml) in combination with
dexamethasone(400mg/0.1 ml) .2-3inj ,2 weekly interval may be
required.
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84.  Azithromycin 250-500mg daily - reduces the rate of recurrence of
retinochoroiditis.(+pyrimethamine+folinic acid+prednisolone)-
Promising newer regimen.
 Atovaquone -750mg (2-4times daily)-attacks encysted bradyzoites
but doesn’t prevent the recurrence.
 Topical steroid and mydriatic may be given for anterior uveitis.
 Antimicrobial maintanence therapy- in immunocomprimised
individuals.
 In pregnancy-
 Intravitreal therapy.
 Systemic treatment with azithromycin+clindamycin+prednisolone
 Congenital toxoplasmosis-
Antimicrobial therapy for 1year may reduce the frequency of
subsequent development of retinochoroidal scars.
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85. ONCHOCERCIASIS
 Onchocerciasis or river blindness is caused by infestation
with the parasitic helminth Onchocerca volvulus.
 The vector is the Black fly Simulium, an obligate
intermediate host, which breeds in fast flowing water.
 It is endemic in West, Central and East Africa, with small
foci in central and South America.
 Microfilariae are mobile and may reach the eye through
the blood stream.
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86. OCULAR FEATURES OF ONCHOCERCIASIS
1. Anterior segment involvement includes :- sclerosing keratitis and
anterior uveitis that may result in pearshaped pupillary dilatation.
2. Live floating microfilariae may be seen in the anterior chamber .
3. In the posterior segment, there is attenuation and perivascular
sheathing of the choroidal vessels.
4. It is slowly progressive & severity may vary from atrophy and
clumping of the RPE to widespread chorioretinal atrophy.
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87. TREATMENT
 Ivermectin is given to eradicate the microfilariae(but not the
adult worm).
 Prophylactic prednisolone is considered in patients with visible
anterior chamber microfilariae.
 Anterior uveitis responds to steroids but the chorioretinal
lesions are irreversible.
 Moxidectin-newer drug
 Doxycycline-100-200mg/day for 6 weeks targets wolbachia-
indirectly preventing microfilarial embryogenesis.
 Suramin-effective against adult worms-given intravenously.
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88. CYSTICERCOSIS
 Cysticercosis refers to a parasitic infestation by Cysticercus
cellulosae, the larval form of the pork tapeworm Taenia
solium.
 Pigs are the intermediate hosts .
 Humans are the definitive hosts .
 Humans acquire the disease by ingesting cysts of T. solium
from contaminated pork, vegetables or water.
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89.  The clinical presentation of ocular cysticercosis depends on two
distinct processes-
 The mass effect and
 The inflammatory response induced at the site of infection.
 It may affect any portion of the visual pathways from the orbit to the
visual cortex
 The live cysticercus present in the vitreous cavity or located
subretinally causes little reaction .But the death of the organism
releases toxins which produce a severe uveitis which may even lead
to endophthalmitis.
 In most cases Ocular cysticercosis is accompanied by cysticercus
infection in the brain, therefore a CT or MRI of the brain should
always be performed.
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90. TREATMENT
 Medical treatment should not be given in intraocular
cysticercosis as violent inflammation following death of the
cyst after drug therapy can lead to loss of the eye with pthysis
bulbi.
 Surgical removal of intravitreal and subretinal cyst by
vitrectomy is the tretament of choice.
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91. S.NO AGE DIAGNOSIS
1. CHILDREN Toxocariasis ,
<16yrs-parasitic uveitis
2. YOUNG ADULTS Non infective uveitis
3. OLD AGE HZ ophthalmicus,TB,leprosy
S.NO CLINICAL SIGNS AND SYMPTOMS CONDITION
1. Prolonged fever,cough,chills,night
sweats,weight loss
Tuberculosis
2. H/O STD,10 chancre, 20 rash, 30-
fever,malaise,joint pains.
Syphilis
3. Immunocomprimised ,exposure to cats,h/o
eating raw meat
Toxoplasmosis
4. Recent tick bite Lyme disease
5. H/o vesicular rash with dermotomal
distribution
HS virus 1,2
HZV
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92. S.NO SYSTEMIC SIGNS CONDITION
1. Loss of hair Syphilis
2. Madarosis Leprosy
3. Hypopigmentation of skin Leprosy
4. Rash syphilis
5. Erythema nodosum TB,leprosy
6. Scaling of skin Syphilis
7. Discoid lesions Leprosy,TB
8. Oral and genital lesions Syphilis
9. Cartilage loss Leprosy,syphilis
10. Lymphnodes TB
11. Respiratory symptoms TB
12. Urethral discharge Syphilis, herpes simplex
13. Epididymitis TB
14. Nephritis TB
15. Neuropathy Leprosy,HZ,sarcoidosis,
syphilis
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93. REFERENCES:-
 Principles and practice of ophthalmology –by Peyman’s.
 Clinical Ophthalmology–A Systematic Approach 8th edition
by Jack J Kanski .
 Uveitis: Fundamentals and Clinical Practice 3rd edition by
Robert B.Nussenblatt.
 Principles and practice of ophthalmology,3rd edition by
Albert and jacobiec’s
 Parson’s Diseases of the Eye-22nd edition .
 Biswas et al(1993) “Practical concepts in the management of uveitis”,indian
journal of ophthalmology,41(3),133-141.
 Rathinam et al(2003) “Algorithmic approach in the diagnosis of uveitis
Indian Journal of Ophthalmology, 61(6), 255.
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94. THANK YOU
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