Tuberculous uveitis is caused by Mycobacterium tuberculosis and can involve the anterior segment, intermediate uveitis, posterior segment, or neuro-ophthalmic structures. Clinical manifestations vary and include anterior uveitis with mutton-fat keratic precipitates, choroidal tubercles appearing as yellow lesions, serpiginous-like choroiditis appearing as multifocal inflammatory lesions, and retinal vasculitis appearing as perivascular infiltrates. Diagnosis involves clinical evaluation, testing for tuberculosis infection via tuberculin skin test or IGRA, and therapeutic trial with antituberculosis medications. Treatment involves a multidrug regimen over a prolonged period to prevent resistance.

1. BACTERIAL UVEITIS-
OCULAR TB
Dr. Rakshya Basnet
2nd year resident
NAMS,LEIRC
1

2. LAYOUT
• Tubercululosis
-introduction
-epidemiology
-pathology
-clinical features
-Diagnosis
-Treatment
• Syphillis
• leprosy
2

3. Bacterial uveitis
•Tuberculosis
•Syphillis
•Leprosy
•Cat scratch disease
•Lyme disease
•Brucellosis
•Leptospirosis
•Whipple disease
•Nocardiosis
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4. TUBERCULOUS UVEITIS
4

5. INTRODUCTION
 Tuberculosis is a chronic infection caused by
Mycobacterium tuberculosis that is characterized by
formation of necrotizing granulomas
 Tuberculosis primarily involves lung
 Other organs including eye may be involved secondarily
5

6. Introduction
caused by three species of mycobacteria
1. M. tuberculosis
2. M. africanum
3. M. bovis
4. M.microti
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7. EPIDEMIOLOGY
• 2 billion people or 1/3rd of world’s population are infected by TB
• 95% of these in developing countries
• 10% of infected are symptomatic
• 80% cases have pulmonary TB
• 20% have extrapulmonary TB
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8. Epidemiology-NEPAL
 Tuberculosis Prevalence Survey (TBPS) 2018-19, jointly
carried out by the National TB programme, Government of
Nepal; with support from World Health Organization (WHO)
 around 117,000 people are living in Nepal with TB
 Every day in Nepal, around 15 people lose their lives to TB,
and over 180 people fall ill
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9. TB &HIV
• TB is most common opportunistic infection in HIV –
positive patients in many developing countries
• In 2009,1.7 million people died from TB, including
380000 people with concomitant HIV infection, which
equates about 4700 deaths /day
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10. Ocular tuberculosis
• Infection by MTB in eye, around eye or on its surface
• Is usually not associated with pulmonary TB as 60% of
extrapulmonary TB patient may not have pulmonary TB
10

11. Types of ocular TB
Primary
• If eye is initial port of entry
• Conjunctival, corneal &scleral disease
Secondary
• Organism spread to eye hematogeously
• Uveal tract,retina,optic nerve
11
Not same as systemic primary and secondary TB

12. Basic mechanism of ocular infection
1. Most common is hematogenous spread
2. Primary exogenous infection of eye, rare,
esp.lids,conjunctiva,cornea,sclera & lacrimal sac
3. Secondary infection from exogenous source of adnexa,
conjunctiva, cornea,sclera
4. Hypersensitivity reaction to mycobacteria present in distant foci
12

13. PATHOLOGY
Bacilli invade tissues
Delayed HSVR
Tubercular granuloma forms
(central caseous necrosis surrounded by epitheloid cells,
Langerhans cells giant cells ,lymphocytes & plasma cells)
In immunocompromised, necrotic & viable neutrophils
mixed with macrophage with numerous bacteria
15

14. PATHOLOGY
16

15. Ocular Manifestations
• Often there is detectable systemic disease,
but eye disease also can occur without
clinically evident extraocular TB
• incidence of tuberculous ocular involvement in
systemic TB is 1% to 2%
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16. CLINICAL PRESENTATION
A) ADNEXALMANIFESTATIONS
B) ANTERIOR SEGMENT MANIFESTATION
C) POSTERIOR SEGMENT MANIFESTATIONS
D) NEURO-OPHTHALMIC MANIFESTATIONS
E) DRUG-RELATED OCULAR TOXICITY IN TB- INFECTED PATIENTS
19

17. A) ADNEXAL MANIFESTATIONS
1) Lupus Vulgaris
2) Eyelid Tuberculous Granuloma
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18. B) ANTERIOR SEGMENT INVOLVEMENT
1) Tuberculous conjunctivitis
2) Conjunctival granuloma
3) Phlyctenular keratoconjunctivitis
4) Tuberculous episcleritis& Scleritis
5) Interstitial keratitis
6) Iridocyclitis
21

19. C) POSTERIOR SEGMENT MANIFESTATIONS
The ocular changes can be divided into four groups:
a. Choroidal tubercles
b. Choroidal tuberculoma
c. Serpiginous like choroiditis
d. Subretinal abscess
22

20. D) NEURO-OPHTHALMIC MANIFESTATIONS
 optic neuropathy develops either from direct infection induced by
mycobacteria or from a hypersensitivity to infectious agent
 involvement may manifest as an optic nerve tubercle, papillitis,
papilledema, optic neuritis, retrobulbar neuritis, neuroretinitis
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21. UVEITIS IN TUBERCULOSIS
33

22. ANTERIOR UVEITIS
• usually is granulomatous and is characterized by
mutton-fat keratic precipitates
Koeppe and Busacca nodules
Iris or angle granuloma
Hypopyon can occur
• possibility of TB should be entertained for any
steroid nonresponsive uveitis
34

23. ANTERIOR UVEITIS
35

24. INTERMEDIATE UVEITIS
 Chronic, low-grade, vitritis with snowball opacities,
snow banking, peripheral vascular sheathing, and
peripheral granuloma.
37

25. POSTERIOR MANIFESTATIONS OF TB
39

26. 1) CHOROIDAL TUBERCLES
 Most common manifestation
of intra-ocular tuberculosis and result from hematogenous spread
 less than 5 upto 50 in number, unilateral or bilateral,
Gray, white to yellow in color with indistinct borders,
are located mostly in posterior pole
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27. FFA
41

28. 2) CHOROIDAL TUBERCULOMA
 Choroidal tubercle continues to
grow, it forms a solitary mass known
tuberculoma
 Present as a solitary, yellowish,
subretinal mass with surrounding
exudative retinal detachment,
mimicking a choroidal tumor
 May be located anywhere
 Measure from 4 to 14 mm in size
43

29. 44
TUBERCULOMA

30. CHOROIDAL TUBERCULOMA
May occur in immunocompetent patients and in patients with
disseminated tuberculosis, may have overlying hemorrhages, retinal folds,
and surrounding exudative retinal detachment
 respond well to antituberculosis treatment
45

31. 3) SERPIGINOUS LIKE CHOROIDITIS
47

32. SERPIGINOUS LIKE CHOROIDOITIS
 bilateral, chronic, progressive and recurrent
inflammation
either solitary or multifocal
solitary are diffuse and plaque-like
multifocal are discrete and initially
noncontigious
48

33. 50
SERPIGINOUS LIKE CHOROIDITIS(SLC) SERPIGINOUS CHOROIDOPATHY(SC)
Infectious etiology Autoimmune and non-infectious
Vitritis common Vitritis uncommon
Usually unilateral Usually bilateral
Treat with ATT mainly Treat with steroid and IMT

34. 51
SLC & CSC

35. FAF (Fundus AutoFluorescence)
52

36. 53
FFA & ICG

37. 4.SUBRETINAL ABSCESS
 Multiplication of bacilli in caseous material
of granulomas can lead to liquefaction
necrosis and abscess formation and form
yellowish subretinal mass lesions
accompanied by exudative retinal
detachment.
 Patients with disseminated tuberculosis
54

38. RETINAL VASCULITIS
 in patients with tuberculosis involve veins or,
rarely, arteries
 characteristic features include bilateral,
vitreous infiltrates (vitritis), perivascular
cuffing,infiltrates, retinal haemorrhages,
perivascular choroiditis scars, neo-
vascularization and neuro-retinitis
56

39.  On FFA, extensive peripheral
capillary nonperfusion areas that lead to retinal/optic
disc neovascularization characterize
TB retinal vasculitis
 It has been long speculated that
patients of idiopathic retinal vasculitis, the so called Eales'
disease, may indeed be tuberculous retinal vasculitis
 presence of MTB DNA was demonstrated in
epiretinal membranes of patients with Eales' disease who
underwent vitreous surgery
57

40. E)DRUG-RELATED OCULAR TOXICITY IN TB- INFECTED PATIENTS
1 ) Ethambutol
 Ocular toxic effects include optic neuritis, colour vision
abnormalities and visual field defects
 Toxicity typically occurs within 3–6 months of starting treatment
61

41. 2) Rifampicin - orange-red discoloration of tears
2) Isoniazid
Optic neuritis
Steven Johnson syndrome involving lids and conjunctiva
 4) Rifabutin used for treatment of pulmonary tuberculosis may in itself
cause anterior uveitis
62

42. DIAGNOSIS
64

43. DIAGNOSIS
I. Clinical signs
II. Ocular investigations
III. Systemic investigations
IV. Exclusion of other uveitis entities
V. Therapeutic test
VI. New diagnostic assays
65

44. I.CLINICAL SIGNS
 Presence of features of any one of following:
uveitis, cyclitis, choroiditis, retinitis ,retinal vasculitis, neuroretinitis,
optic neuropathy, endophthalmitis and panophthalmitis
 An intractable disease course with multiple recurrences on
nonspecific treatment (corticosteroids) is a clue suggesting a
possible tubercular etiology
66

45. II. OCULAR INVESTIGATIONS
a. Demonstration of AFB by microscope or culture of M.
tuberculosis from intraocular fluid/tissue-media
b. Positive polymerase chain reaction from
intraocular fluids
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46. III.SYSTEMIC INVESTIGATION
a. Positive Mantoux reaction
b. Evidence of healed or active tubercular lesion on radiography of
chest
c. Evidence of confirmed active extrapulmonary tuberculosis (either by
microscopic examination or by culture of affected tissue for M
tuberculosis)
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47. MOUNTOUX TEST
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48. Mantoux test
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49. 71
INTERPRETATION

50. Chest x-ray
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51. IV. EXCLUSION OF OTHER UVEITIC INCLUSIONS
Other causes of uveitis must be excluded by various laboratory
investigations including serology for syphilis, toxoplasmosis,sarcoidosis,
and others.
73

52. D.THERAPEUTIC TEST
 A positive response to 4-drug ATT (isoniazid, rifampicin, ethambutol,
and pyrazinamide) over a period of 4 to 6 weeks can be diagnostic.
 Therapeutic trial with single drug isoniazid should be avoided due
to risk of development of resistance.
74

53. NEW DIAGNOSTIC TESTS
Interferon-g release assays (IGRA)
 It based on the in vitro assays that measure interferon-g released
by sensitized T cells after stimulation by Mycobacterium
tuberculosis antigens.
 Two kits are available commercially:
 TSPOT. TB test
 QuantiFERON —TB GOLD
75

54. Quantiferon TB GOLD (QFT)
• simple blood test that aids in the detection of MTB
• modern alternative to Mantoux
• controlled laboratory test that requires only one patient visit and
is unaffected by previous BCG vaccination
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55. GENE XPERT
• CBNAAT (catridge based nucleic acid amplification test)
77

56. • detection of Mycobacterium Tuberculosis in early stage where
direct smear is negative
• early detection of Rifampicin resistance
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57. TREATMENT
 complex ,high levels of patient adherence are required.
 Inappropriate management can result in life-threatening
consequences as well as drug resistance
 multiple drug regimen is recommended to avoid resistance.
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58. 81

59. Treatment
For uncomplicated pulmonary and extrapulmonary TB, recommended
treatment is
 INH + rifampicin + ethambutol + pyrazinamide first 2 months, R+I
for 4 mths
 In disseminated TB, TB meningitis, and TB in AIDS, INH plus rifampicin
plus ethambutol (or pyrazinamide) should be given for at least 9
months
The World Health Organization is recommending “directly observed treatment,
short course” (DOTS) to cure 95% of all TB
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60. 83

61. 84

62. 85

63. 86

64. DRUG RESISTANT TB
87

65. MDR-TB
- Resistance to Isoniazid and rifampicin
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66. XDR-TB
 Resistance to Isoniazid+rifampicin+any one of
fluroquinolone+at least one injectable drug of second line
89

67. Corticosteroids in Treatment
• Systemic corticosteroids also may be needed to
preserve vision in which severe intraocular
inflammation is caused by ocular TB for 4-6 weeks
together with ATT limit damage by delayed HSVR
90

68. • dose of corticosteroid should be as low as possible to
avoid immunosuppression and infection flare-up
• One should consider use of sub-Tenon's corticosteroids
in these patients to avoid use of systemic
corticosteroids
• Topical corticosteroids can be used safely for anterior
uveitis, interstitial keratitis & phlyctenulosis
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69. COMPLICATIONS OF OCULAR TB
 Corneal Scarring
 Cataract
 Glaucoma
 Vitreous hemorrhage
 Subretinal fibrosis
 CNV
 Cystoid Macular edema
 Retinal detachment
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70. SYPHILITIC UVEITIS
94

71. Syphilis is caused by bacterium Treponema pallidum
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72. Transmission
• sexually transmitted disease
• transfusion of fresh blood
• accidental contact with an infected lesion
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73. SYSTEMIC ASSOCIATIONS
3 clinical stages:
Primary stage
• is characterized by an ulcerative lesion called a chancre
• Occurs in site where Tr. pallidum penetrates skin or
mucous membrane
• Organism enters lymphatics and blood stream &
disseminates shortly after contact
99

74. Secondary stage
• fever,malaise, lymphadenopathy,& mucocutaneous lesions
• Clinically apparent secondary syphilis occurs in 60–90% of
patients,& one third of patients who have secondary syphilis
may have primary chancre as well
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75. Tertiary stage
• refers to its late sequelae
• Complications-vaso vasorum of aorta or CNS
• Focal inflammatory lesions, known as gummas, may
affect any organ
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76. 1 . Primary syphilis
 Eye chancre (Conjunctival chancre)
OCULAR SYPHILIS
102

77. 2 . Secondary
 Orbit and eyelids
 Eyelid rash
 Orbital periostitis
 Dacryocystitis
 Dacryoadenitis
 Madarosis
 Anterior segment
 Conjunctivitis
 Interstitial keratitis
 Episcleritis, scleritis
 Uveitis
 Posterior segment
 Chorioretinitis
 Neuroretinitis
 Retinal vasculitis
 Neuroophthalmic
 Optic neuritis
 CN palsies
OCULAR SYPHILIS
103

78. 3 . Tertiary
 Anterior segment findings similar to secondary syphilis
(interstitial keratitis, uveitis etc.)
 Lens subluxation
 Neuroophthalmic
Pupils
 Argyll Robertson pupil
 Tonic pupils
 Homer's syndrome
 RAPD (optic atrophy)
 Others
 CN palsies
 Ptosis
 Nystagmus
 VF defects
 Gumma of ocular structures
OCULAR SYPHILIS
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79. Uveitis
• Nonspecific iritis and iridocyclitis
• granulomatous or nongranulomatous
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80.  dilated iris vessels (iris roseolae)
 iris atrophy
 posterior synechiae
 lens dislocation
106

81. Posterior uveitis:
• most common variant
• painless but may cause severe vision loss.
• 75% have chorioretinitis
• 15% panuveitis
• 10% retinal vasculitis
107

82. Chorioretinitis
2 types of chorioretinitis:
MULTI/ UNI FOCAL
108

83. posterior placoid chorioretinitis:
-affects optic disc or macular region and is limited to RPE:
macular or juxtapapillary
-placoid yellowish or grey lesions with faded centres, at
level of RPE, accompanied by vitritis.
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84. Retinitis:
• choroidal involvement
• commonly affecting posterior pole
• characterized by focal areas of retinal edema, vasculitis,
papillitis, & vitritis necrotizing retinitis in midperiphery and
peripheral retina
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85. Retinal vasculitis
• affecting any retinal vessel
• FA: obliteration of vessels from occlusive vasculitis BRVO
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86. Keratouveitis
• uveitis and corneal involvement together may be seen
Uveitic complications
• exudative/serous retinal detachment and glaucoma may
occur
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87. 114

88. 115

89. TREATMENT
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90. 117

91. LEPROSY
•Mycobacterium leprae
•Spreads by nasal secretions
•Highest incidence of ocular complication among all systemic
bacterial infection
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92. stages
2 stages
1. Mycobacterial
2. immune
119

93. Ocular manifestation
1) Adnexal
• Madarosis
• ectropion
• entropion
• triachiasis
• decreased blinking
• paralytic lagophthalmos
120

94. 2) Ocular surface
• Corneal hypoesthesia
• corneal nerve beading
• dry eyes
• exposure keratitis
• secondary infectious keratitis
• corneal scarring
121

95. 3) Intraocular
• Chronic granulomatous iridocyclitis
• diffuse iris atropy
• iris pearls
• miotic pupils
• complicated cataract
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96. Diagnosis
• hypopigmented or reddish skin lesions
• definite sensory loss
• with or without thickened peripheral nerves
• and acid-fast bacilli identified on skin smears or biopsy samples
123

97. TREATMENT
124

98. BIBLIOGRAPHY
• American academy of ophthalmology, intraocular inflammation and
uveitis, 2016-2017
• Myron yanoff- Duker ophthalmology-4th edition
• Jack j kanski, Brad Bowling , clinical ophthalmology-9th edition
• Diagnosis & Treatment of uveitis Foster & Vitale
• Journals
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99. THANK YOU 182