Trachoma ....whatever you need basic !

1. Dr. Nitish Narang

2. • Trachoma was previously known as 'Egyptian
ophthalmia'. The word trachoma comes from
the greek word for 'rough ‘
• It is a chronic conjunctival inflammation
caused by infections with serotypes A , B , Ba ,
and C of chlamydial trachomatis.
• Currently trachoma is the 2nd
leading cause of preventable
blindness.

3.  Etiology :
Trachoma is caused by chlamydia trachomatis
belonging to the Psittacosis-Lymphogranuloma-
trachoma {PLT} group.
The organism is epitheliotropic and produces
intracytoplasmic inclusion bodies { halberstaedter
prowazeke bodies }.
Presently 11 serotypes of chlamydia
{ A,B,Ba,C,D,E,F,G,H,J and K }

4.  Serotypes A , B , Ba , and C are
associated with hyperendemic { blinding
trachoma } or nonblinding trachoma {in
hypoendemic areas}
 Serotypes D-K are associated with
paratrachoma {oculogenital chlamydial
disease}.Mostly seen in urban
population and manifest as adult
inclusion conjunctivitis.

6. Predisposing factors:
Age : during infancy and early childhood.
Otherwise there is no age bar.
Sex : more common in females.
Climate : more common in dry and dusty
weather.
Socioeconomic status : more common in poor
classes due to unhygienic living conditions,
overcrowding, unsanitary conditions,
abundant fly population, paucity of water and
others.

7. Source of infection:
• In trachoma endemic zones the main source
of infection is the conjunctival discharge of
the affected person.
• Therefore, superimposed bacterial infections
help in transmission of the disease by
increasing the conjunctival secretions.
• Incubation period : 5 to 12 days

8. Modes of infection:
Infections may spread from eye to eye by
any of the following modes:
 Direct spread of infections occurs through contact
by airborne or waterborne infections.
 Vector transmission of trachoma is common
through flies. The housefly is Musca domestica of
the order Diptera.
 Material transfer play an important role in the
spread of trachoma. Material transfer can occur
through contaminated finger of doctors, nurses and
contaminated tonometers. Other sources of
material transfer of infection are use of common
towel, handkerchief, bedding and surma rods.

10. Prevalance

12. • Trachoma is a worldwide disease but it is
highly prevalent in NorthAfrica, MiddleEast
and certain regions of SouthEast Asia.
• About 6 million people currently suffer from
irreversible blindness due to trachoma in
Africa and Asia.
• Another 152 million suffer from the disease
and need treatment and about 540 million
are at risk of infection.
It is estimated to be responsible for 0.2% of
visual impairment and blindness in India.

14. Clinical profile of trachoma
• Natural history of trachoma :
 Blinding trachoma, the end stage of a chronic
process is caused by repeated infections with
chlamydia trachomatis, occurs in impoverished
population living under conditions of poor
hygeine.
 In hyperendemic areas, infection is acquired
during infancy and most children are infected by
2 yrs of age.

15.  Primary infection induces purulent follicular
conjunctivitis { except during neonatal period}
 The follicles consist of lymphoid germinal
centers. Because lymphoid tissue is absent
from the conjunctiva of neonates, lymphoid
follicles do not form in them.
 Primary infection resolves spontaneously
and induces transient protective immunity, in
endemic areas however reinfection is
inevitable.

16.  The same serovar of CT is often
transmitted reciprocally among members
of a household.
 With repeated inf, healing is associated
with central degeneration and necrosis of
lymphoid follicles, thinning of the overlying
conjunctival epithelium and proliferation of
fibroblast, resulting in fibrosis and scarring.

17.  Uninterrupted progression of this process
eventually converts the normal smooth
and lubricating conjunctival epithelium in
to one that is xerotic and cicatrized.
 Extensive fibrosis produces entropion and
trichiasis
 End stage blindness is the result of corneal
drying, ulceration and scarring.

18. Pathogenesis:
 The observation that repeated chlamydial
infections are characteristic of the course of
blinding trachoma has led to the concept that the
disease constitutes an immunopathologic
response of the host to the CT infection.
 Initial infection presumably induces immune
sensitization of the host but only transient or
incomplete protective immunity.
 Reinfection or relapse results in intensified
inflammatory rtx, fibrosis, scarring and pannus
formation.

19. • Consistent with this observation is a report
that trachoma did not progress further in
persons who moved from an endemic to an
nonendemic area where they were no longer
exposed to the pathogens.
• Immunopathogenesis is further evidenced by
the finding that in trachoma endemic areas,
proliferative response of peripheral blood
lymphocytes to stimulation by chlamydial
antigens, a marker of CMI, are more common
in pts with trachoma than in controls.

20. • The apparent genetic susceptibility to
trachoma further supports this concept.
• In a study done in Gambia, the frequencies
of the HLA Complex Class 1 antigen, HLA-
A28 and A’6808 allele were significantly
greater in pts with trachoma than in age,
sex and location matched controls.

21. Signs and Symptoms:
 symptoms :
 In the absence of secondary infection,
symptoms are minimal and include mild
foreign body sensation, occasionally
lacrimation, slight stickiness of the lids and
scanty mucoid discharge.
 In the presence of secondary infection,
typical sym of acute mucopurulent
conjunctivitis develop.

22. Signs:
 A. Conjunctival signs:
1.Congestion of upper tarsal and forniceal
conjunctiva.
2.Conjunctival follicles: These are
commonly seen on upper tarsal
conjunctiva and fornix, but may also be
present in the lower fornix. Sometimes
follicles may be seen on the bulbar
conjunctiva { path gnomic of trachoma }

23. • Follicles are yellowish white, discrete, round
elevations of conjunctiva produced by
lymphocytic response.
• Central portion of the follicle is avascular with
blood vessels sweeping over the convexity from
the base.
• Typically 0.5 to 2.0mm in diameter.
• Follicles are lymphoid germinal centers with
fibroblast in the center and large multinucleated
cells called Leber cells.
• Presence of Leber cells and signs of necrosis
differentiate trachoma follicles from other
follicular conjunctivitis.

24. • 3. Papillary hyperplasia: characterized by
folds or projections of hypertrophic
epithelium that contains a central fibro
vascular core whose blood vessels arborize
on reaching the surface.
• It results from edema and PMN cell
infiltration of the conjunctiva.

25. • 4. Conjunctival scarring: may be irregular, star
shaped or linear. Linear scar presents in the
sulcus subtarsalis is called ‘ Arlts line ‘.
• 5. Concretions may be due to accumalation of
dead epithelial cells and inspissated mucus.

26. • B. corneal signs:
• 1. Superficial keratitis may be present in
the upper part.
• 2. Herbert follicles refers to typical follicles
present in the limbal area
• 3. Pannus ie infiltration of the cornea
associated with vascularization in the
upper part.

27. • In pannus the vessels are superficial and lie
between epithelium and bowmans
membrane. Later on bowmans membrane is
also destroyed.
Pannus may be progressive or regressive.
o In progressive pannus, infiltration of cornea is
ahead of vascularization.
o In regressive pannus vessels extends a short
distance beyond the area of infiltration.

28. • 5. Herbert pits are the oval or circular
pitted scars, left after healing of herbert
follicles in the limbal area.
• 6. Corneal ulcer may sometimes develop at
the advancing edge of pannus.
• 7. Corneal ulcer may be present in the
upper part. It may even extend down and
involve the pupillary area. It’s the end
result of trachomatous corneal lesions.

29. A) WHO grade TF (trachomatous inflammation, follicular). To make a
diagnosis of WHO grade TF, five or more white or yellow follicles >0.5
mm must be visualized on the upper tarsal conjunctiva. B) Herbert's
pits. Herbert's pits are shallow pits in the cornea that form as a
result of follicle rupture. They are pathognomonic for trachoma but are
not assessed in the current grading scheme.

30. Grading of trachoma:
• Mc Callans classification:
4 stages:
Stage 1- Incipient trachoma or stage of
infiltration. It is characterized by hyperaemia of
palpebral conjunctiva and immature follicles.
Stage 2- Established trachoma or stage of florid
infiltration . It is characterized by appearance of
mature follicles, papillae and progressive corneal
pannus.
Stage 3- cicatarizing trachoma or stage of scarring .
Obvious scarring of palpebral conjunctiva.
Stage 4- healed trachoma or stage of sequale.

31. • Who classification :
suggested by WHO in 1987 .{ FISTO }

33. Clockwise from top left:
follicles of trachoma (TF), intense inflammation
of trachoma (TI), trichiasis of trachoma (TT),
conjunctival scarring of trachoma

34. Sequelae of trachoma
• Sequale in the lids –
Trichiasis, entropion, tylosis { thickening of
the lid margin }, ptosis, madrosis and
ankyloblepharon.
• Conjunctival Sequale-
Concretions, pseudocyst, xerosis and
symblepharon.
• Corneal Sequale-
Corneal opacity, ectasia, corneal xerosis and
total corneal pannus [blinding sequale]

35.  Diagnosis :
For the purpose of diagnosis cases must
have at least 2 of the following diagnostic
criteria:
1.Follicles on the upper tarsal conjunctiva.
2.Limbal follicles and their sequalae, herberts
pits.
3.Typical conjunctival scarring{ trichiasis,
entropion }
4.Vascular pannus, most marked at the superior
limbus.

36.  Laboratory diagnosis:
1.Conjunctival cytology: giemsa stained smear
shows a predominantly PMN rtx with
presence of plasma cells and leber cells.
2.Detection of inclusion bodies: in conjunctival
smear may be possible by giemsa stain, iodine
stain or immunofluorescent staining, specially
in cases with active trachoma.
3.ELISA for chlamydial antigens.
4.PCR.
5.Microimmunoflurescence method to detect
specific antibodies.
6.Direct monoclonal ab micrscopy of
conjunctival smear is rapid and inexpensive.

38. • Differential diagnosis:
Trachoma with follicular hypertrophy:
must be differentiated with acute adenoviral
follicular conjunctivitis.
• Distribution of follicles in trachoma is mainly
on upper palpebral conjunctiva and fornix,
while in EKC lower palpebral conjunctiva and
fornix is predominantly involved.
• Associated signs like pannus and papillae.
• Lab diagnosis of trachoma.

39. Trachoma with predominant papillary
hypertrophy:
must be differentiated from spring catarrh.
• Papillae are large in size and usually there
is typical cobblestone appearance in SC.
• pH of tears is usually alkaline in spring
catarrh, while in trachoma its acidic.
• Discharge is ropy in spring catarrh.
• In trachoma there is associated follicles
and pannus.

40. Management:
Includes curative as well as control measures
 Treatment of active trachoma.
• Antibiotics for active trachoma may be given
locally or systemically.
• Azithromycin 1gm PO stat is now standard
drug for prevention and eradication.
• Other drugs used are
Tetracycline or erytromycin 250mg po qid for
4 weeks OR
Doxycycline 100mg po BD for 4 weeks.

41. Problems with antibiotics
 Antibiotics have side effects
 Overuse can make people immune to
them. For this reason they should only be
part of trachoma treatment, used with
infection-reduction methods such as facial
cleanliness and good sanitation.
 Treatment takes a long time and is
difficult to administer in rural areas

42. Topical therapy regimes:
Best for individual cases and is usually
preferred because-
• It is cheaper.
• No risk of systemic side effects.
• Local antibiotics are also effective against
bacterial conjunctivitis which may be
associated with trachoma.

43. • Topical therapy regimens.
1% tetracycline or 1% erythromycin eye
ointment QID for 6 weeks.
Or
20% sulfacetamide eye drops 3 times a day
along with 1% tetracycline oint HS for 6
weeks.

44. Treatment of sequelae
 Concretions should be removed with a
hypodermic needle.
 Trichiasis may be treated by epilation,
electrolysis or cryolysis.
 Entropion should be corrected surgically.
 Xerosis should be treated by artificial tears.

46. Prophylaxis:
• Since immunity is very poor and short lived,
so reinfections and recurrences are likely to
occur. Following prophylactic measures
may be helpful against reinfection.
• Hygienic measures: trachoma is closely
associated with personal hygeine and
environmental sanitations.
Therefore health education on trachoma
should be given to public.

47. • The use of common towels, handkerchief,
surma rods etc should be discouraged.
• A good environmental sanitation
will reduce the flies.
• A good water supply would
improve washing habits.

48.  The housefly has been brought under control
in many areas by good sewerage systems,
garbage disposal, and other elimination of its
breeding places.
 Houseflies are also brought under control
through the use of insecticides.
 Protection of food by the use of screens,
refrigerators, and covered containers has
checked the spread of disease by houseflies.

49. Early treatment of conjunctivitis:
every cases should be treated as early as possible
to reduce transmission of disease.
Blanket antibiotic therapy { intermittent
treatment }
WHO has recommended this regimen to be
carried out in endemic areas to minimize the
intensity and severity of disease.
The regimen is to apply
1% tetracycline oint BD for 5
days in a month for
6 months.

50. • Prevention of trachoma blindness:
Effective measures have been taken in
developing nations using the SAFE stratergy:
Surgery to correct lid deformity
and prevent blindness.
Antibiotics for acute infections
and community control.
Facial hygiene.
Environmental changes
including improved access
to water and sanitation and
health education.

51.  Elimination of blindness due to trachoma is
considered feasible, eradication of
trachoma is not .
 WHO has organized an alliance for Global
Elimination of Trachoma by the year 2020
{GET 2020}.