Symptoms of leprosy eye organ

Prior to the widespread use of sulfonamides, damage to the organ of vision in leprosy occurred in a large percentage of cases: 77.4% in each case. No other infectious disease had such a high incidence of eye damage. Currently, in connection with the success of therapy and prevention of leprosy, the disease of the organ of vision is observed much less frequently: according to U. Ticho, J. Sira (1970) - 6.3%, A. Patel and J. Khatri (1973) - 25 , 6% of cases. However, among the untreated patients, the specific inflammation of the eyes and its subsidiary organs, according to the observations of A. Patel, J. Khatri (1973), is 74.4%.

The organ of vision in leprosy patients is involved in the pathological process only a few years after the onset of the disease. Inflammation of the eyes and its subsidiary organs is observed with all types of leprosy, most often with lepromatous. In this case, changes in the eye's auxiliary organs (eyebrows, eyelids, eyeballs, teardrop, conjunctiva), fibrous, vascular and reticular membranes of the eyeball and optic nerve are detected.

Leprosy lesion of the secondary organs of the eye. A change in the skin in the region of the superciliary arches is observed simultaneously with the inflammatory process of the facial skin and serves as one of the early clinical manifestations of leprosy. Specific inflammation of the skin of the superciliary region is detected with all types of leprosy, most often with lepromatous. In this case, diffuse lepromatous infiltration and isolated dermal and hypodermal leproms are noted. Erythematous skin spots in the area of the superciliary arches are rare. In the affected areas of the skin, focal anesthesia, dilatation of the excretory ducts and secretion of the sebaceous glands, and the absence of sweating are detected. At the site of resorbed leprom and diffuse infiltrates of the skin, there are atrophic scars. At the same time, there is a rarefaction, and then a complete and persistent loss of the eyebrows, caused by dystrophic changes in the perifollicular nerves. Scarify from the affected areas of the skin of the superciliary arches find mycobacteria leprosy.

Defeat of the skin of the eyelids is observed with all types of leprosy, most often with lepromatous. Specific inflammation of the skin of the eyelids is manifested more often in the form of diffuse and less often - limited infiltration. Lepromy skin of the eyelids is localized mainly along the ciliary edge of the eyelids or near it. Localized hypo- and anesthesia, violation of the functions of the sebaceous and sweat glands, are found in the zone of lepromatous infiltrates and leprom. Sedation and scarring of diffuse infiltrates and leprom skin of the eyelids and their edges leads to the formation of atrophic scars of the skin and the wrong position of the eyelids. Due to lepromatous infiltration of the edges of the eyelids and dystrophic changes in the perifollicular nerves, a rarefaction is observed, followed by a complete and persistent loss of eyelashes. In scarifications from the affected sites, the eyelids are determined by mycobacteria leprosy.

In addition to specific inflammation of the skin of the eyelids, lupus patients may have a lesion of the circular muscle of the eyelids, which leads to their non-closure. Laphophthalmia is most common in undifferentiated lepera. The cause of the defeat of the circular muscle of the eyelids is its progressive amyotrophy due to paresis or paralysis of the facial nerve. The earliest symptoms of the change in the circular muscle of the eyelids are fibrillar twitching, eyelid twitching when they are closed, and rapidly onset muscle fatigue with blinking eyelid movements. Simultaneously with the uncovering of the optic cleft, the lumbar punctures are reversed, and then the inversion of the lower eyelids is observed. Due to the inconsistency of the eyelids and the anesthesia of the cornea, keratitis develops.

Along with the lagophthalmus, paralytic ptosis may be observed in some cases, in others - the widening of the eye gap. Omission of the upper eyelid by 3-4 mm is due to a decrease in the tone m. Levator palpebrae superioris and m. Tarsalis superior. The widening of the optic gap by 3-6 mm is due to a disbalance between the circular muscle of the eyelids and the muscle lifting the upper eyelid.

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

Lacrimal apparatus with a leprosy process suffers comparatively rarely. Having begun acutely with the expressed painful syndrome, the inflammation of the lacrimal gland proceeds chronically and is accompanied by a decrease to the complete cessation of tear formation. When lesions of the tear ducts are observed obliteration of lacrimal points and tubules, inflammation of the lacrimal sac. Mycobacterium leprosy is found in the walls of the lacrimal sac. Some authors deny the leprosy etiology of dacryocystitis.

Specific conjunctivitis is more often diagnosed with lepromatous type of disease. Leprosy conjunctivitis is always bilateral and proceeds more often in the form of diffuse catarrhal inflammation with hyperemia, edema, diffuse infiltration of the mucous membrane of the eyeball, eyelids and a slight mucopurulent discharge. Less common nodular leprosy conjunctivitis. Focal infiltrates (nodules) are localized mainly on the conjunctiva of the eyelids near the ciliary margin. The causative agent of leprosy is very rarely found in the conjunctival sac and in scarifications from the mucous membrane of the eyeball and the eyelids. A distinctive feature of specific conjunctivitis in leprosy patients is an arecative (caused by hypo- or anesthesia of the conjunctiva) and a chronic recurrent course.

Leprosy lesion of the fibrous membrane of the eyeball. Specific episcleritis and sclerites are, as a rule, bilateral and are observed mainly in patients with lepromatous type of leprosy. Initially, the epicler is affected, then the sclera is involved in the inflammatory process. Scleral disease, as a rule, develops simultaneously with the defeat of the cornea, iris and ciliary body.

Leprosy episcleritis and sclerites can be diffuse and nodular. Currently diffuse episclerites and sclerites are more often observed, the course of which is comparatively favorable. They begin to 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 episcler end in partial or complete resolution of inflammatory infiltration or scarring and thinning of the sclera. In a number of cases (with the transformation of one clinical type of leprosy into another) it can turn into a nodular one.

Nose sclerites begin to acutely. Lepromes often localize at the beginning of the limb, then the inflammatory process extends to the cornea, iris and ciliary body. In these cases, lepromatosis of the entire anterior section of the eyeball develops, and sometimes all its membranes with the outcome in the subatrophy of the eye. In other cases, there may be a resorption of scleral leproms, their scarring with the formation of intercalary staphylomas. With histological examination, sclera and episcler are found in a large number of mycobacterium leprosy. The course of nodular episcleritis and scleritis is chronic, relapsing.

Thus, for specific leprosy episcleritis and sclerites, a frequent combination with cornea, iris and ciliary disease, a chronic and recurrent course are common. It is possible to transform diffuse inflammation into nodular inflammation.

In previous years, the defeat of the cornea in patients with leprosy with eye disease was observed very often - 72.6%. At present, there is a decrease in the incidence of leprosy keratitis and a more benign course of them. The cornea is affected by all types of leprosy, more often with lepromatous. With lepromatous, tuberculoid and borderline forms, keratitis is specific, with nondifferentiated nonspecific, as it develops as a result of a lagophthalmus. Specific keratitis, as a rule, bilateral.

The appearance of inflammatory infiltration in the cornea is preceded by a change in her pain and tactile sensitivity and a thickening of the nerves of the cornea. The decrease in the sensitivity of the cornea is primarily determined in its peripheral parts (when examined with Frey's hair). In the central part of the cornea, normal sensitivity persists significantly longer. Hypo- and anesthesia of the cornea is caused by dystrophic changes in the trigeminal nerve. When biomicroscopy is predominantly near the limb in the upper-arm segments, the thickening of the nerves of the cornea in the form of shiny nodules is found. These limited thickening of the corneal nerves are pathognomopic for leprosy eye damage. With histological examination, perineural infiltration is determined in them.

Specific keratitis can be diffuse and nodular. A heavier current is noted with nodular keratitis. With diffuse inflammation of the cornea develops sclerosing or diffuse-vascular, with limited - point or nodular keratitis.

With sclerosing keratitis near the focal infiltration of the sclera, the limb is defined by the turbidity of the deep layers of the cornea. In the zone of turbidity, focal hypo- or anesthesia is noted, and sometimes a few newly formed vessels. The centers of deep infiltration of the cornea are never ulcerated. The course of the disease is anactive, chronic with periodic exacerbations, accompanied by the appearance of new foci of opacity in the deep layers of the cornea.

With diffuse vascular keratitis, the process usually begins in the upper third of the cornea and gradually spreads to the greater part of the cornea. In the deep layers of the cornea, diffuse inflammatory infiltration and a significant number of newly formed vessels are observed. Leprosy pannus cornea differs from trachomatous by the deep location of the newly formed vessels. Infiltration of the cornea in diffuse-vascular keratitis is never ulcerated. The sensitivity of the cornea is reduced or completely absent. The course of the disease is anactive, chronic with periodic exacerbations.

With pinpoint keratitis, usually in the upper third of the cornea, point infiltrates are found, located predominantly in the middle layers, respectively, of the localization of the thickened nerves of the cornea. Hypo- or anesthesia of the cornea is noted. Development of newly formed vessels is not observed. Histological studies indicate that point corneal infiltrates are miliary leproms. The course of the disease is reactive, chronic, recurrent.

Nodal leprosy keratitis is the most severe, acute leaking form of specific keratitis. It is observed during the development of leprosy reactions, i.e. With exacerbation of the disease. Usually in the upper limb area there are leproms of dense consistency, soldered to bulbar conjunctiva. The inflammatory process progresses, spreads over most of the corneal stroma, iris and ciliary tissue. Leukemia remains on the site of the corneal lesions that have been healed. In severe cases, the inflammatory process extends to all the shells of the eyeball with an outcome in its atrophy. The disease progresses with periodic exacerbations.

With an undifferentiated type of leprosy due to lesions of the facial and trigeminal nerve, leading to the development of lagophthalmia, anesthesia and disruption of corneal trophism, keratitis lagophthalmo can be observed. Infiltrates are located in the superficial layers of the cornea. The epithelium covering them is often rejected, corneal erosions are formed. Keratitis of this type proceeds inactive, chronically with periodic exacerbations. Due to violation of corneal trophism, such dystrophic keratitis as ribbon, circular, bullous can also be observed.

Thus, keratitis, which is the most common clinical form of eye leprosy, proceeds mainly "reactively, chronically with periodic exacerbations. The above described types 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. The clinical feature of specific keratitis in leprosy patients 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 mycobacterium leprosy in the cornea with bacterioscopic and histological studies.

[1], [2], [3], [4]

Leprosy lesion of the choroid of the eyeball

Irradiation of the iris and ciliary body (as a rule, bilateral) are observed in all types of leprosy, most often with lepromatous. The frequency of specific irites and iridocyclitis in patients with leprosy with eye diseases, according to different 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, resulting from focal infiltration of the iris stroma and the branches of the nerves innervating the dilator, the pupil sphincter and the ciliary muscle. Uneven pupil contraction is observed in case of strong illumination, periodically arising anisocoria due to dilatation of the pupil of one or the other eye, weakening or total absence of pupillary responses to light, accommodation and convergence, weak dilatation of pupils after the installation of 1% solution of atropine sulfate. There is also an irregular shape of the pupils. Due to the paresis of the ciliary muscle, patients can present asthenopic complaints during visual work at close range.

Leprosy inflammation of the iris and ciliary body is diffuse and localized. The course is predominantly chronic with periodic exacerbations. Morphological features distinguish serous, plastic, miliary and nodose irites and iridocyclites.

Serous irites and iridocyclites develop sluggishly, accompanied by edema of the iris, clouding of the moisture in the anterior chamber of the eye. Sometimes the appearance of small corneal precipitates and increased intraocular pressure. The course of the disease is anactive, chronic with periodic exacerbations.

Plastic irites and iridocyclitis are also characterized by a flaccid course, marked by fibrinous exudation, early formation of anterior and posterior synechia, up to the occlusion of the pupil, leading to the development of secondary glaucoma. In the exudate of the anterior chamber of the eye, mycobacteria of leprosy can be detected. The course of the disease is reactive, chronic, relapsing.

Patognomonichnym for leprosy is a billionth irit, flowing without symptoms of eye irritation. On the front surface of the iris (more often in the pupil, sometimes in the ciliary belt) small (with the millet grain) round shape of a snow-white color, shiny, usually multiple rashes (nodules), resembling pearls are determined. With the arrangement of miliary nodules in the stroma of the iris, its surface becomes uneven, bumpy. According to histological studies, miliary eruptions of the iris are miliary leproms. In the moisture of the anterior chamber of the eye, floating microparticles formed during the decay of miliary leprom in the iris can be contained. The course of the disease is anactive, chronic, progressive with periodic exacerbations.

The most severe clinical manifestations of inflammation of the iris and ciliary body in leprosy patients 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), various sizes of rounded nodules of yellow-gray color are determined. According to the histological examination, they are specific granulomas (leproms). Nodular iritis, iridocyclitis, as a rule, is combined with damage to the cornea and sclera, sometimes complicated cataract develops. Lepromes of the iris and the ciliary body can resolve, however, in the tissues there remain foci of destruction. In the iris, such a stromal defect leads to the exposure of the pigmentary leaf. In the unfavorable course of the process, inflammatory infiltration extends to the entire uveal tract with an outcome in the atrophy of the eyeball. The course of the disease is progressive with periodic exacerbations.

A distinctive feature of leprosy irites and iridocyclites is their long, progressive and areactive (with the exception of nodose form) flow. Symptoms of eye irritation are observed only during an exacerbation of the inflammatory process in the eye. The defeat of the iris and ciliary body is often combined with the disease of the cornea and sclera. The clinical forms of iritium and iridocyclitis, the degree of their manifestation and the development of exacerbations are associated with the type and nature of the leprosy in the patient. Mixed clinical forms of damage to the iris and ciliary body (a combination of diffuse and localized irites and iridocyclitis) and the transition of one clinical form to another are also observed. At histological researches in a iris and the ciliary body are determined mycobacteria leprosy.

With prolonged specific iridocyclitis, according to the data of some authors, bilateral bias of the lens is noted in 12.6% of cases. Cataract is complicated and develops due to the toxic effects of general and local leprosy infection. Specific inflammatory infiltration and destruction of the lens capsule can be observed. In cataract masses, mycobacteria leprosy are sometimes found. In a number of cases, a cataract is formed by resolution of the cataract masses.

Leprosy lesion of the retina of the eye and optic nerve. Changes in the fundus in patients with leprosy lesions of the organ of vision, unlike those in tuberculous and leukemic infections, are rare: according to the data of Yu. I. Garus (1961) - 5.4%, A. Hornbeass (1973) - 4% . Defeat of the retina is observed with all forms of leprosy, but mainly with lepromatous. It is noted as an isolated lesion of the retina, and combined (most often) disease of the retina and the vascular membrane proper. Usually, on the extreme periphery of the fundus of both eyes, small round shapes with sharply outlined borders of white or yellow-white foci resembling pearls or droplets of stearin are determined. Retinal and chorioretinal foci poorly pigmented. Retinal vessels are intact. P. Metge et al. (1974) found pronounced changes in the retinal vessels. The appearance of fresh inflammatory foci on the eye bottom with the deterioration of the general leprosy process is sometimes accompanied by the development of opacity of the vitreous.

The question of the specific etiology of changes in the fundus in leprosy patients has 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 leprosy and specific changes in the retina and the actual choroid of the eye. Chorioretinal foci are leproms. In some cases, inflammatory changes in the fundus are combined with specific lesions of the anterior part of the eyeball. At the periphery of the fundus, in the region of the macula and peripapillary, dystrophic changes can also be observed-cystic, colloidal retinal dystrophy.

Leprosy lesions of the optic nerve are rarely diagnosed, mainly in patients with lepromatous leprosy. Specific optic neuritis, as a rule, ends with its atrophy. With histological examination, the mycobacteria of leprosy are found in the optic nerve.

The degree of reduction in 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 whole organism and the retina, oppression of the light and color sensitive apparatus of the eye is often manifested in concentric narrowing of the peripheral boundaries of the field of vision to white and chromatic objects, widening the boundaries of the blind spot and reducing dark adaptation. NM Pavlov (1933) determined a decrease in the dark adaptation in patients with leprosy as a "light anesthesia" of the retina.

Thus, the damage to the organ of vision is found 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 leprosy in the patient. Before widespread use of sulfones, leprosy damage to the organ of vision was observed in 85% of patients and was most often detected with lepromatous type of leprosy. At present, the disease of the organ of vision of leprosy etiology is found in 25.6% of the treated I in 74.4% of untreated patients.

The clinical forms of leprosy of the organ of vision are diverse and are characterized by a predominant lesion of the anterior part of the eyeball and its auxiliary organs. Mixed clinical forms (keratoscleritis, keratoiridocyclitis, etc.) are often observed. In this case, a specific inflammation can be diffuse (flowing more favorably) or nodose. When transforming tuberculoid leprosy into lepromatous diffuse inflammation of the tissues of the eyeball and its auxiliary organs, it can pass into a nodular one.

The leprosy etiology of damage to the organ of vision is confirmed by bacterioscopic and histological studies. During bacterioscopic examination, the lepra causative agent was detected 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. In histological examination, mycobacterium leprosy was found in the external muscles of the eyeball, cornea, sclera and episclera, iris, ciliary body, the vascular membrane, the lens, the retina and the optic nerve.

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

In conclusion, it should be noted that the incidence and severity of lesions of the eye in treated leprosy patients in the past two decades has fallen dramatically. With timely treatment, inflammatory changes in the shell of the eye and its subsidiary organs are not detected or have a favorable course and outcome.