Symptoms of lepra of the visual organ

Before the widespread use of sulfone drugs, damage to the organ of vision in leprosy occurred in a large percentage of cases: 77.4%. Such a high frequency of eye damage was not observed in any other infectious disease. At present, due to the success of therapy and prevention of leprosy, disease of the organ of vision is observed much less frequently: according to U. Ticho, J. Sira (1970) - in 6.3%, A. Patel and J. Khatri (1973) - in 25.6% of cases. However, among untreated patients, specific inflammation of the eye and its accessory organs, according to observations of A. Patel, J. Khatri (1973), is 74.4%.

The organ of vision in patients with leprosy is involved in the pathological process only several years after the onset of the disease. Inflammation of the eyes and their accessory organs is observed in all types of leprosy, most often in lepromatous leprosy. In this case, changes are detected in the accessory organs of the eye (eyebrows, eyelids, muscles of the eyeball, lacrimal apparatus, conjunctiva), fibrous, vascular and retinal membranes of the eyeball and optic nerve.

Leprosy lesion of accessory organs of the eye. Changes in the skin in the area of the superciliary arches are observed simultaneously with the inflammatory process of the skin of the face and is one of the early clinical manifestations of leprosy. Specific inflammation of the skin of the superciliary region is detected in all types of leprosy, most often in lepromatous leprosy. In this case, diffuse lepromatous infiltration and isolated dermal and hypodermal lepromas are noted. Erythematous spots of the skin in the area of the superciliary arches are rare. In the affected areas of the skin, focal anesthesia, expansion of the excretory ducts and increased secretion of the sebaceous glands, and lack of sweating are found. Atrophic scars remain at the site of resolved lepromas and diffuse skin infiltrates. At the same time, rarefaction is noted, and then complete and persistent loss of eyebrows, caused by dystrophic changes in the perifollicular nerves. Mycobacterium leprae is found in scarifications from affected areas of the skin of the superciliary arches.

Skin lesions of the eyelids are observed in all types of leprosy, most often in lepromatous leprosy. Specific inflammation of the eyelid skin is more often manifested as diffuse and less often as limited infiltration. Lepromas of the eyelid skin are localized mainly along the ciliary margin of the eyelids or near it. In the area of lepromatous infiltrates and lepromas, local hypo- and anesthesia, dysfunction of the sebaceous and sweat glands are found. Resorption and scarring of diffuse infiltrates and lepromas of the skin of the eyelids and their edges leads to the formation of atrophic scars of the skin and an abnormal position of the eyelids. Due to lepromatous infiltration of the eyelid margins and dystrophic changes in the perifollicular nerves, rarefaction and then complete and persistent loss of eyelashes are observed. Mycobacterium leprae are determined in scarifications from the affected areas of the eyelid scars.

In addition to specific inflammation of the skin of the eyelids, patients with leprosy may have damage to the orbicularis oculi muscle, which leads to their failure to close. Lagophthalmos is most often found in undifferentiated leprosy. The cause of damage to the orbicularis oculi muscle is its progressive amyotrophy due to paresis or paralysis of the facial nerve. Early symptoms of changes in the orbicularis oculi muscle are fibrillary twitching, tremors of the eyelids when they close, and rapid fatigue of the muscle during blinking movements of the eyelids. Simultaneously with the failure to close the palpebral fissure, eversion of the lower lacrimal points is observed, and then eversion of the lower eyelids. Keratitis develops due to failure to close the eyelids and anesthesia of the cornea.

Along with lagophthalmos, paralytic ptosis may be observed in some cases, and in others, widening of the palpebral fissure. Drooping of the upper eyelid by 3-4 mm occurs due to decreased tone of m. levator palpebrae superioris and m. tarsalis superior. Widening of the palpebral fissure by 3-6 mm is caused by an imbalance between the orbicularis oculi muscle and the muscle that lifts the upper eyelid.

In patients with leprosy with inflammatory changes in the visual organ, lesions of the external muscles of the eyeball may be observed, accompanied by diplopia and ophthalmoplegia. During histological examination, mycobacteria of lepra were found in the external muscles of the eye.

The lacrimal apparatus suffers comparatively rarely in the leprosy process. Having begun acutely with a pronounced pain syndrome, inflammation of the lacrimal gland proceeds chronically and is accompanied by a decrease up to a complete cessation of lacrimation. When the lacrimal ducts are affected, obliteration of the lacrimal points and canals, inflammation of the lacrimal sac are observed. Mycobacterium leprae are detected in the walls of the lacrimal sac. Some authors deny the leprosy etiology of dacryocystitis.

Specific conjunctivitis is more often diagnosed in the lepromatous type of the disease. Leprosy conjunctivitis is always bilateral and usually occurs as diffuse catarrhal inflammation with hyperemia, edema, diffuse infiltration of the mucous membrane of the eyeball, eyelids and minor mucopurulent discharge. Nodular leprosy conjunctivitis is less common. Focal infiltrates (nodules) are localized mainly on the conjunctiva of the eyelids near the ciliary edge. The causative agent of leprosy is very rarely detected in the discharge from the conjunctival sac and in scarifications from the mucous membrane of the eyeball and eyelids. A distinctive feature of specific conjunctivitis in patients with leprosy is an arective (caused by hypo- or anesthesia of the conjunctiva) and chronic relapsing course.

Leprosy lesion of the fibrous membrane of the eyeball. Specific episcleritis and scleritis are usually bilateral and are observed mainly in patients with the lepromatous type of leprosy. The episclera is affected first, then the sclera is involved in the inflammatory process. Disease of the sclera, as a rule, develops simultaneously with damage to the cornea, iris and ciliary body.

Leprosy episcleritis and scleritis can be diffuse or nodular. Currently, diffuse episcleritis and scleritis are more often observed, the course of which is comparatively favorable. They begin sluggishly, proceed for a long time with periodic exacerbations. Inflammatory infiltration of the sclera has a light yellow color, reminiscent of the color of ivory. Diffuse inflammation of the sclera and episclera ends with partial or complete resorption of inflammatory infiltration or scarring and thinning of the sclera. In some cases (with the transformation of one clinical type of leprosy into another), it can turn into nodular.

Nodular scleritis begins acutely. Lepromas are often localized initially in the limbus, then the inflammatory process spreads to the cornea, iris and ciliary body. In these cases, lepromatosis of the entire anterior part of the eyeball develops, and sometimes all its membranes with an outcome in subatrophy of the eye. In other cases, resorption of scleral lepromas, their scarring with the formation of intercalary staphylomas can be observed. Histological examination reveals a large number of mycobacteria leprae in the sclera and episclera. The course of nodular episcleritis and scleritis is chronic, recurrent.

Thus, specific leprosy episcleritis and scleritis are characterized by frequent combination with damage to the cornea, iris and ciliary body, chronic and recurrent course. Transformation of diffuse inflammation into nodular is possible.

In previous years, corneal lesions in patients with leprosy and eye disease were observed very often - 72.6%. Currently, there is a decrease in the frequency of leprosy keratitis and a more benign course. The cornea is affected in all types of leprosy, more often in lepromatous. In lepromatous, tuberculoid and borderline leprosy, keratitis is specific, in undifferentiated leprosy it is nonspecific, since it develops as a result of lagophthalmos. Specific keratitis is usually bilateral.

The appearance of inflammatory infiltration in the cornea is preceded by a change in its pain and tactile sensitivity and thickening of the corneal nerves. A decrease in corneal sensitivity is determined primarily in its peripheral parts (when examined using Frey's hairs). In the central part of the cornea, normal sensitivity is preserved much longer. Hypo- and anesthesia of the cornea are caused by dystrophic changes in the trigeminal nerve. Biomicroscopy reveals bead-like thickenings of the corneal nerves in the form of shiny nodules, mainly at the limbus in the upper outer segments. These limited thickenings of the corneal nerves are pathognomopic for leprosy eye disease. Histological examination reveals perineural infiltration in them.

Specific keratitis can be diffuse and nodular. A more severe course is observed with nodular keratitis. With diffuse inflammation of the cornea, sclerosing or diffuse-vascular develops, with limited - point or nodular keratitis.

In sclerosing keratitis, near focal infiltration of the sclera at the limbus, opacity of the deep layers of the cornea is determined. In the opacity zone, focal hypo- or anesthesia is observed, sometimes a few newly formed vessels. Foci of deep infiltration of the cornea never ulcerate. The course of the disease is areactive, chronic with periodic exacerbations, accompanied by the appearance of new foci of opacity in the deep layers of the cornea.

In diffuse vascular keratitis, the process usually begins in the upper third of the cornea and gradually spreads to most of it. In the deep layers of the cornea, diffuse inflammatory infiltration and a significant number of newly formed vessels are observed. Leprous corneal pannus differs from trachomatous pannus by the deep location of newly formed vessels. The corneal infiltrate in diffuse vascular keratitis never ulcerates. Corneal sensitivity is reduced or completely absent. The course of the disease is areactive, chronic with periodic exacerbations.

In punctate leprosy keratitis, punctate infiltrates are usually found in the upper third of the cornea, located mainly in the middle layers according to the localization of thickened corneal nerves. Hypo- or anesthesia of the cornea is noted. Development of newly formed vessels is not observed. Histological studies indicate that punctate corneal infiltrates are miliary lepromas. The course of the disease is areactive, chronic, recurrent.

Nodose leprosy keratitis is the most severe, acute form of specific keratitis. It is observed during the development of leprosy reactions, i.e. during an exacerbation of the disease. Usually, dense lepromas, fused with the bulbar conjunctiva, appear in the area of the upper limbus. The inflammatory process progresses, spreading to most of the corneal stroma, the tissue of the iris and the ciliary body. Leukomas remain in place of the corneal lepromas that have healed. In severe cases, the inflammatory process spreads to all membranes of the eyeball, resulting in its atrophy. The disease progresses with periodic exacerbations.

In the case of undifferentiated leprosy, due to damage to the facial and trigeminal nerves, leading to the development of lagophthalmos, anesthesia and disruption of corneal trophism, keratitis lagophthalmos may be observed. Infiltrates are located in the superficial layers of the cornea. The epithelium covering them is often rejected, and corneal erosions are formed. Keratitis of this type is areactive, chronic with periodic exacerbations. Due to disruption of corneal trophism, such dystrophic keratitis as band-like, circular, and bullous may also be observed.

Thus, keratitis, which is the most common clinical form of leprosy of the eye, proceeds mainly "reactively, chronically with periodic exacerbations. The above-described varieties of leprosy keratitis are not strictly isolated clinical forms, since depending on the tendency of development of the leprosy process, transitions of one form of keratitis to another are possible. A clinical feature of specific keratitis in patients with leprosy is their frequent combination with lesions of the iris and ciliary body. Exacerbations of leprosy keratitis, as a rule, coincide with exacerbations of the general leprosy process. The specific etiology of keratitis is confirmed by the detection of leprosy mycobacteria in the cornea during bacterioscopic and histological studies.

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Leprosy lesion of the choroid of the eyeball

Lesions of the iris and ciliary body (usually bilateral) are observed in all types of leprosy, most often in lepromatous leprosy. The frequency of specific iritis and iridocyclitis in patients with leprosy and eye diseases, according to various authors, ranges from 71.3 to 80%.

Early clinical symptoms of leprosy changes in the iris are impaired pupillary mobility and changes in their shape, which occur as a result of focal infiltration of the iris stroma and branches of the nerves innervating the dilator, sphincter of the pupil, and ciliary muscle. Uneven contraction of the pupils is observed when they are strongly illuminated, periodically occurring anisocoria due to dilation of the pupil of one or the other eye, weakening or complete absence of pupillary reactions to light, accommodation, and convergence, weak dilation of the pupils after instillation of a 1% solution of atropine sulfate. Irregular pupil shape is also observed. Due to paresis of the ciliary muscle, patients may present asthenopic complaints during visual work at close range.

Leprosy inflammation of the iris and ciliary body can be diffuse and localized. The course is predominantly chronic with periodic exacerbations. According to morphological features, serous, plastic, miliary and nodular iritis and iridocyclitis are distinguished.

Serous iritis and iridocyclitis develop sluggishly, accompanied by edema of the iris, clouding of the fluid of the anterior chamber of the eye, sometimes the appearance of small corneal precipitates and increased intraocular pressure. The course of the disease is areactive, chronic with periodic exacerbations.

Plastic iritis and iridocyclitis are also characterized by a sluggish course, pronounced fibrinous exudation, early formation of anterior and posterior synechiae up to occlusion of the pupil, leading to the development of secondary glaucoma. Mycobacterium leprae may be detected in the exudate of the anterior chamber of the eye. The course of the disease is areactive, chronic, recurrent.

Pathognomonic for leprosy is miliary iritis, which occurs without symptoms of eye irritation. On the anterior surface of the iris (usually in the pupillary, sometimes in its ciliary belt) there are small (the size of a millet grain), rounded, snow-white, shiny, usually multiple rashes (nodules), resembling pearls. When miliary nodules are located in the stroma of the iris, its surface becomes uneven and bumpy. According to histological studies, miliary rashes of the iris are miliary lepromas. The fluid in the anterior chamber of the eye may contain floating microparticles formed during the disintegration of miliary lepromas of the iris. The course of the disease is areactive, chronic, progressive with periodic exacerbations.

The most severe clinical manifestations of inflammation of the iris and ciliary body in patients with leprosy are nodular (nodular) iritis and iridocyclitis, which are also pathognomonic for the leprosy process. The disease is acute. In the stroma of the iris (at its base or in the pupillary zone), rounded yellow-gray nodules of various sizes are determined. According to histological examination, they are specific granulomas (lepromas). Nodular iritis and iridocyclitis are usually combined with damage to the cornea and sclera, sometimes complicated cataracts develop. Lepromas of the iris and ciliary body can resolve, but foci of destruction remain in the tissues. In the iris, such a stromal defect leads to the exposure of the pigment sheet. In case of unfavorable course of the process, inflammatory infiltration spreads to the entire uveal tract with the outcome in atrophy of the eyeball. The course of the disease is progressive with periodic exacerbations.

A distinctive feature of leprosy iritis and iridocyclitis is their long, progressive and areactive (except for the nodose form) course. Symptoms of eye irritation are observed only during the period of exacerbation of the inflammatory process in the eye. The lesion of the iris and ciliary body is often combined with the disease of the cornea and sclera. The clinical forms of iritis and iridocyclitis, the degree of their severity and the development of exacerbations are associated with the type and nature of the course of leprosy in the patient. Mixed clinical forms of lesion of the iris and ciliary body (a combination of diffuse and localized iritis and iridocyclitis) and the transition of one clinical form to another are also observed. Mycobacterium leprae are determined in the iris and ciliary body during histological examination.

In long-term specific iridocyclitis, according to some authors, bilateral lens opacity is observed in 12.6% of cases. Cataract is complicated and develops as a result of the toxic effects of general and local leprosy infection. Specific inflammatory infiltration and destruction of the lens capsule may be observed. Mycobacterium leprae are sometimes found in cataractous masses. In some cases, membranous cataract is formed during the resorption of cataractous masses.

Leprosy lesion of the retina and optic nerve. Changes in the fundus of the eye in patients with leprosy lesion of the organ of vision, in contrast to those in tuberculous and luetic infections, are rarely observed: according to Yu. I. Garus (1961) - in 5.4%, A. Hornbeass (1973) - in 4% of cases. Retinal lesion is observed in all forms of leprosy, but mainly in lepromatous leprosy. Both isolated lesion of the retina and combined (most often) disease of the retina and the choroid itself are noted. Usually, small rounded foci with sharply defined borders of white or yellow-white color, resembling pearls or drops of stearin, are determined on the extreme periphery of the fundus of both eyes. Retinal and chorioretinal foci are weakly pigmented. The retinal vessels are intact. P. Metge et al. (1974) found marked changes in the retinal vessels. The appearance of fresh inflammatory foci on the fundus with worsening of the general leprosy process is sometimes accompanied by the development of vitreous opacity.

The question of the specific etiology of changes in the fundus of the eye in leprosy patients remained controversial for many years. G. Hansen and O. Bull (1873), L. Borthen (1899) and others denied the leprosy etiology of retinitis and chorioretinitis in leprosy patients. However, subsequent clinical observations and histological studies confirmed the presence of Mycobacterium leprae and specific changes in the retina and the choroid. Chorioretinal foci are lepromas. In some cases, inflammatory changes in the fundus are combined with specific lesions of the anterior part of the eyeball. Dystrophic changes - cystic, colloid dystrophy of the retina - can also be observed on the periphery of the fundus, in the area of the macula lutea and peripapillary.

Leprosy lesions of the optic nerve are diagnosed rarely, mainly in patients with lepromatous leprosy. Specific neuritis of the optic nerve usually ends in its atrophy. Histological examination reveals mycobacteria of leprosy in the optic nerve.

The degree of reduction of visual acuity and other visual functions depends on the severity and duration of leprosy eye damage. In patients with leprosy, sometimes in the absence of clinical signs of damage to the eyeball due to intoxication of the entire body and retina, suppression of the light- and color-sensitive apparatus of the eye is often detected, expressed in a concentric narrowing of the peripheral boundaries of the field of vision for white and chromatic objects, expansion of the boundaries of the blind spot and a decrease in dark adaptation. N. M. Pavlov (1933) defined a decrease in dark adaptation in patients with leprosy as "light anesthesia" of the retina.

Thus, damage to the organ of vision is detected several years after the onset of the disease and serves as a local manifestation of the general leprosy process. Clinical forms of eye damage, the degree of their severity and the development of exacerbations are associated with the type and nature of the course of leprosy in the patient. Before the widespread use of sulfones, leprosy damage to the organ of vision was observed in 85% of patients and was most often detected in the lepromatous type of leprosy. Currently, eye disease of leprosy etiology is detected in 25.6% of treated and 74.4% of untreated patients.

Clinical forms of leprosy of the visual organ are varied and are characterized by predominant damage to the anterior part of the eyeball and its accessory organs. Mixed clinical forms (keratoscleritis, keratoiridocyclitis, etc.) are often observed. In this case, specific inflammation can be diffuse (proceeding more favorably) or nodose. When tuberculoid leprosy transforms into lepromatous leprosy, diffuse inflammation of the tissues of the eyeball and its accessory organs can become nodular.

The leprosy etiology of the visual organ damage is confirmed by bacterioscopic and histological studies. During bacterioscopic examination, the leprosy pathogen was determined in the discharge from the conjunctival sac, exudate of the anterior chamber of the eye, scarifications from the mucous membrane of the eyeball and eyelids, from the cornea and affected areas of the skin of the superciliary arches and eyelids. During histological examination, leprosy mycobacteria were found in the external muscles of the eyeball, cornea, sclera and episclera, iris, ciliary body, choroid proper, lens, retina and optic nerve.

The course of leprosy disease of the organ of vision is, as a rule, areactive, chronic, progressive with periodic exacerbations that coincide with exacerbations of the general leprosy process.

In conclusion, it should be noted that the frequency and severity of visual organ damage in treated leprosy patients have decreased sharply over the past two decades. With timely treatment, inflammatory changes in the eye membrane and its accessory organs are not detected or have a favorable course and outcome.