Dr. Nitish Narang

• 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.

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 }

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.

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.

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

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.

Prevalance

• 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.

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.

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.

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.

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.

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.

• 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.

• 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.

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.

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 }

• 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.

• 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.

• 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.

• 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.

• 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.

• 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.

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.

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.

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

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

conjunctival scarring of trachoma

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]

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.

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.

• 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.

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.

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.

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

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.

• 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.

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.

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.

• 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.

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.

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.

• 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.

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}.