Trachoma (previously known as Egyptian
ophthalmia) is a chronic keratoconjunctivitis,
primarily affecting the superficial epithelium of
conjunctiva and cornea simultaneously. It is
characterised by a mixed follicular and papillary
response of conjunctival tissue. It is still one of the
leading causes of preventable blindness in the world.
The word 'trachoma' comes from the Greek word for
'rough' which describes the surface appearance of
the conjunctiva in chronic trachoma.
Table 4.2. Summary of ocular infections caused by chlamydia
Genus Chlamydia
Species C. trachomatis C. lymphogranulomatis C. psittacosis
(TRIC agent) (Humans) (Humans) (Animals)
Serotype A, B, Ba, C D to K L1, L2, L3
Ocular Hyperendemic Paratrachoma Lymphogranuloma
disease trachoma (– neonatal venereum
and adult inclusion conjunctivitis
Transmission Eye to eye Genitals to eye Genitals to eye
A. Causative organism. Trachoma is caused by a
Bedsonian organism, the Chlamydia trachomatis
belonging to the Psittacosis-lymphogranulomatrachoma
(PLT) group. The organism is epitheliotropic
and produces intracytoplasmic inclusion bodies
called H.P. bodies (Halberstaedter Prowazeke
bodies). Presently, 11 serotypes of chlamydia, (A, B,
Ba, C, D, E, F, G, H, J and K) have been identified
using microimmunofluorescence techniques.
Serotypes A, B, Ba and C are associated with
hyperendemic (blinding) trachoma, while serotypes
D-K are associated with paratrachoma (oculogenital
chlamydial disease).
B. Predisposing factors. These include age, sex, race,
climate, socioeconomic status and environmental
1. Age. The infection is usually contracted during
infancy and early childhood. Otherwise, there is
no age bar.
2. Sex. As far as sex is concerned, there is general
agreement that preponderance exists in the
females both in number and in severity of disease.
3. Race. No race is immune to trachoma, but the
disease is very common in Jews and comparatively
less common among Negroes.
4. Climate. Trachoma is more common in areas with
dry and dusty weather.
5. Socioeconomic status. The disease is more
common in poor classes owing to unhygienic
living conditions, overcrowding, unsanitary
conditions, abundant fly population, paucity of
water, lack of materials like separate towels and
handkerchiefs, and lack of education and
understanding about spread of contagious
6. Environmental factors like exposure to dust,
smoke, irritants, sunlight etc. increase the risk of
contracting disease. Therefore, outdoor workers
are more affected in comparison to office workers.
C. 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.
D. Modes of infection. Infection may spread from
eye to eye by any of the following modes:
1. Direct spread of infection may occur through
contact by air-borne or water-borne modes.
2. Vector transmission of trachoma is common
through flies.
3. Material transfer plays an important role in the
spread of trachoma. Material transfer can occur
through contaminated fingers of doctors, nurses
and contaminated tonometers. Other sources of
material transfer of infection are use of common
towel, handkerchief, bedding and surma-rods.
Trachoma is a worldwide disease but it is highly
prevalent in North Africa, Middle East and certain
regions of Sourth-East Asia. It is believed to affect
some 500 million people in the world. There are about
150 million cases with active trachoma and about 30
million having trichiasis, needing lid surgery.
Trachoma is responsible for 15-20 percent of the
world's blindness, being second only to cataract.
Clinical profile of trachoma
Incubation period of trachoma varies from 5-21 days.
Onset of disease is usually insidious (subacute),
however, rarely it may present in acute form.
Clinical course of trachoma is determined by the
presence or absence of secondary infection. In the
absence of such an infection, a pure trachoma is so
mild and symptomless that the disease is usually
neglected. But, mostly the picture is complicated by
secondary infection and may start with typical
symptoms of acute conjunctivitis. In the early
stages it is clinically indistinguishable from the
bacterial conjunctivitis and the term 'trachomadubium'
(doubtful trachoma) is sometimes used for
this stage.
Natural history. In an endemic area natural history
of trachoma is characterized by the development of
acute disease in the first decade of life which
continues with slow progression, until the disease
becomes inactive in the second decade of life. The
sequelae occur at least after 20 years of the disease.
Thus, the peak incidence of blinding sequelae is seen
in the fourth and fifth decade of life.
64 Comprehensive OPHTHALMOLOGY
In the absence of secondary infection, symptoms
are minimal and include mild foreign body
sensation in the eyes, occasional lacrimation,
slight stickiness of the lids and scanty mucoid
In the presence of secondary infection, typical
symptoms of acute mucopurulent conjunctivitis
A. Conjunctival signs
1. Congestion of upper tarsal and forniceal
2. Conjunctival follicles. Follicles (Fig. 4.9 and
Fig.4.10) look like boiled sagograins and are
commonly seen on upper tarsal conjunctiva and
fornix; but may also be present in the lower
fornix, plica semilunaris and caruncle. Sometimes,
(follicles may be seen on the bulbar conjunctiva
(pathognomic of trachoma).
follicular conjunctivitis.
3. Papillary hyperplasia. Papillae are reddish, flat
topped raised areas which give red and velvety
appearance to the tarsal conjunctiva (Fig. 4.11).
Each papilla consists of central core of numerous
dilated blood vessels surrounded by lymphocytes
and covered by hypertrophic epithelium.
Fig. 4.10. Trachomatous inflammation follicular (TF)
Structure of follicle. Follicles are formed due to
scattered aggregation of lymphocytes and other
cells in the adenoid layer. Central part of each follicle
is made up of mononuclear histiocytes, few
lymphocytes and large multinucleated cells called
Leber cells. The cortical part is made up of a zone
of lymphocytes showing active proliferation. Blood
vessels are present in the most peripheral part. In
later stages signs of necrosis are also seen. Presence
of Leber cells and signs of necrosis differentiate
trachoma follicles from follicles of other forms of
Fig. 4.9. Signs of active traochoma (diagramatic).
Fig. 4.11. Trachomatous inflammation intense (TI)
4. Conjunctival scarring (Fig. 4.12), which may be
irregular, star-shaped or linear. Linear scar present
in the sulcus subtarsalis is called Arlt's line.
5. Concretions may be formed due to accumulation
of dead epithelial cells and inspissated mucus in
the depressions called glands of Henle.
Fig. 4.12. Trachomatous scarring (TS)
Fig. 4.13. Trachomatous pannus : (A) progressive,
(B) regressive (diagramatic) and (C) clinical photograph
B. Corneal signs
1. Superficial keratitis may be present in the upper
2. Herbert follicles refer to typical follicles present
in the limbal area. These are histologically similar
to conjunctival follicles.
3. Pannus i.e., infiltration of the cornea associated
with vascularization is seen in upper part (Fig.
4.13). The vessels are superficial and lie between
epithelium and Bowman's membrane. Later on
Bowman's membrane is also destroyed. Pannus
may be progressive or regressive.
In progressive pannus, infiltration of cornea is
ahead of vascularization.
In regressive pannus (pannus siccus) vessels
extend a short distance beyond the area of
4. Corneal ulcer may sometime develop at the
advancing edge of pannus. Such ulcers are usually
shallow which may become chronic and indolent.
5. Herbert pits are the oval or circular pitted
scars, left after healing of Herbert follicles in the
limbal area (Fig. 4.14).
6. Corneal opacity may be present in the upper
part. It may even extend down and involve the
pupillary area. It is the end result of trachomatous
corneal lesions.
Grading of trachoma
McCallan's classification
McCallan in 1908, divided the clinical course of the
trachoma into following four stages:
Stage I (Incipient trachoma or stage of infiltration).
It is characterized by hyperaemia of palpebral
conjunctiva and immature follicles.
Stage II (Established trachoma or stage of florid
infiltration). It is characterized by appearance of
mature follicles, papillae and progressive corneal
Fig. 4.14. Trachomatous Herbert's pits.
66 Comprehensive OPHTHALMOLOGY
Stage III (Cicatrising trachoma or stage of
scarring). It includes obvious scarring of palpebral
Stage IV (Healed trachoma or stage of sequelae).
The disease is quite and cured but sequelae due
to cicatrisation give rise to symptoms.
WHO classification
Trachoma has always been an important blinding
disease under consideration of WHO and thus many
attempts have been made to streamline its clinical
profile. The latest classification suggested by WHO
in 1987 (to replace all the previous ones) is as follows
1. TF: Trachomatous inflammation-follicular. It is
the stage of active trachoma with predominantly
follicular inflammation. To diagnose this stage at
least five or more follicles (each 0.5 mm or more
in diameter) must be present on the upper tarsal
conjunctiva (Fig. 4.10). Further, the deep tarsal
vessels should be visible through the follicles
and papillae.
2. TI : Trachomatous inflammation intense. This
stage is diagnosed when pronounced
inflammatory thickening of the upper tarsal
conjunctiva obscures more than half of the normal
deep tarsal vessels (Fig. 4.11).
3. TS: Trachomatous scarring. This stage is
diagnosed by the presence of scarring in the
tarsal conjunctiva. These scars are easily visible
as white, bands or sheets (fibrosis) in the tarsal
conjunctiva (Fig. 4.12).
4. TT: Trachomatous trichiasis. TT is labelled when
at least one eyelash rubs the eyeball. Evidence of
recent removal of inturned eyelashes should also
be graded as trachomatous trichiasis (Fig. 4.15).
5. CO: Corneal opacity. This stage is labelled when
easily visible corneal opacity is present over the
pupil. This sign refers to corneal scarring that is
so dense that at least part of pupil margin is
blurred when seen through the opacity. The
definition is intended to detect corneal opacities
that cause significant visual impairment (less than
Sequelae of trachoma
1. Sequelae in the lids may be trichiasis (Fig. 4.15),
entropion, tylosis (thickening of lid margin), ptosis,
madarosis and ankyloblepharon.
Fig. 4.15. Trachomatous trichiasis (TT).
2. Conjunctival sequelae include concretions,
pseudocyst, xerosis and symblepharon.
3. Corneal sequelae may be corneal opacity, ectasia,
corneal xerosis and total corneal pannus (blinding
4. Other sequelae may be chronic dacryocystitis,
and chronic dacryoadenitis.
The only complication of trachoma is corneal ulcer
which may occur due to rubbing by concretions, or
trichiasis with superimposed bacterial infection.
A. The clinical diagnosis of trachoma is made from
its typical signs; at least two sets of signs should be
present out of the following:
1. Conjunctival follicles and papillae
2. Pannus progressive or regressive
3. Epithelial keratitis near superior limbus
4. Signs of cicatrisation or its sequelae
Clinical grading of each case should be done as
per WHO classfication into TF, TI, TS, TT or CO.
B. Laboratory diagnosis. Advanced laboratory tests
are employed for research purposes only. Laboratory
diagnosis of trachoma includes :
1. Conjunctival cytology. Giemsa stained smears
showing a predominantly polymorphonuclear
reaction with presence of plasma cells and Leber
cells is suggestive of trachoma.
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. Enzyme-linked immunosorbent assay (ELISA) for
chlamydial antigens.
4. Polymerase chain reaction (PCR) is also useful.
5. Isolation of chlamydia is possible by yolk-sac
inoculation method and tissue culture technique.
Standard single-passage McCoy cell culture
requires at least 3 days.
6. Serotyping of TRIC agents is done by detecting
specific antibodies using microimmunofluorescence
(micro-IF) method. Direct
monoclonal fluorescent antibody microscopy of
conjunctival smear is rapid and inexpensive.
Differential diagnosis
1. Trachoma with follicular hypertrophy must be
differentiated from acute adenoviral follicular
conjunctivitis (epidemic keratoconjunctivitis) as
follows :
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 such as papillae and pannus
are characteristic of trachoma.
In clinically indistinguishable cases, laboratory
diagnosis of trachoma helps in differentiation.
2. Trachoma with predominant papillary
hypertrophy needs to be differentiated from palpebral
form of spring catarrh as follows:
Papillae are large in size and usually there is
typical cobble-stone arrangement in spring catarrh.
pH of tears is usually alkaline in spring catarrh,
while in trachoma it is acidic,
Discharge is ropy in spring catarrh.
In trachoma, there may be associated follicles
and pannus.
In clinically indistinguishable cases, conjunctival
cytology and other laboratory tests for trachoma
usually help in diagnosis.
Management of trachoma should involve curative as
well as control measures.
A. Treatment of active trachoma
Antibiotics for treatment of active trachoma may be
given locally or systemically, but topical treatment is
preferred because:
It is cheaper,
There is no risk of systemic side-effects, and
Local antibiotics are also effective against
bacterial conjunctivitis which may be associated
with trachoma.
The following topical and systemic therapy
regimes have been recommended:
1. Topical therapy regimes. It is best for individual
cases. It consists of 1 percent tetracycline or 1
percent erythromycin eye ointment 4 times a day
for 6 weeks or 20 percent sulfacetamide eye
drops three times a day along with 1 percent
tetracycline eye ointment at bed time for 6 weeks.
The continuous treatment for active trachoma
should be followed by an intermittent treatment
especially in endemic or hyperendemic area.
2. Systemic therapy regimes. Tetracycline or
erythromycin 250 mg orally, four times a day for
3-4 weeks or doxycycline 100 mg orally twice
daily for 3-4 weeks or single dose of 1 gm
azithromycin has also been reported to be equally
effective in treating trachoma.
3. Combined topical and systemic therapy regime.
It is preferred when the ocular infection is severe
(TI) or when there is associated genital infection.
It includes: (i) 1 per cent tetracycline or
erythromycin eye ointment 4 times a day for 6
weeks; and (ii) tetracycline or erythromycin 250
mg orally 4 times a day for 2 weeks.
B. Treatment of trachoma sequelae
1. Concretions should be removed with a
hypodermic needle.
2. Trichiasis may be treated by epilation, electrolysis
or cryolysis (see page 348).
3. Entropion should be corrected surgically (see
page 349).
4. Xerosis should be treated by artificial tears.
C. 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 of trachoma.
1. Hygienic measures. These help a great deal in
decreasing the transmission of disease, as
trachoma is closely associated with personal
68 Comprehensive OPHTHALMOLOGY
hygiene and environmental sanitation. Therefore,
health education on trachoma should be given to
public. The use of common towel, handkerchief,
surma rods etc. should be discouraged. A good
environmental sanitation will reduce the flies. A
good water supply would improve washing habits.
2. Early treatment of conjunctivitis. Every case of
conjunctivitis should be treated as early as
possible to reduce transmission of disease.
3. Blanket antibiotic therapy (intermittent
treatment). WHO has recommended this regime
to be carried out in endemic areas to minimise the
intensity and severity of disease. The regime is
to apply 1 percent tetracycline eye ointment twice
daily for 5 days in a month for 6 months.
D. Prevention of trachoma blindness
See page 447.

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