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Leptospirosis of the eye: causes, symptoms, diagnosis, treatment
Last reviewed: 05.07.2025
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[ Causes and epidemiology of ocular leptospirosis
The causative agents of leptospirosis are spirochetes leptospira. The sources of leptospira in nature are rodents, some domestic animals (cows, pigs, dogs, etc.). They excrete leptospira with urine and feces, polluting the soil, water bodies, food products, and household items. People become infected mainly when swimming, drinking water, less often through contaminated food products, and sometimes when caring for sick animals. Leptospira penetrate the human body through the mucous membrane of the mouth, gastrointestinal tract, easily damaged skin, and conjunctiva, without causing a local inflammatory reaction. Leptospirosis can be sporadic, but endemics and epidemics are possible, especially the so-called bathing epidemics in June-September. Currently, there is no distinction between icteric and anicteric forms of the disease, since they have the same pathogenetic essence and anicteric forms can occur with jaundice.
Pathogenesis of leptospirosis of the eyes
Leptospira are hematogenously distributed to organs containing reticuloendothelial tissue and multiply in them. Then they enter the blood again, causing hyperthermia and intoxication. In response to this, antibodies are produced. The destruction of leptospira occurs with the release of toxic products, which is manifested by toxemia. Anemia, jaundice, and hemorrhagic syndrome develop due to damage to the capillary endothelium. In addition, in response to the disintegration of leptospira, the accumulation of endogenous biologically active products, sensitization of the body occurs, allergic reactions occur. In the 2nd-3rd week of leptospirosis, antibodies accumulate in the blood, due to which the pathogen disappears from the blood, concentrating in organs and tissues (non-sterile immunity). During this period, complications may be observed in the eyes, nervous system, kidneys, liver, etc. Inflammatory and dystrophic processes develop in them, functions are impaired. Subsequently, leptospirosis agglutinins accumulate in the blood, ensuring the disappearance of the pathogen (sterile immunity).
Symptoms of Leptospirosis of the Eyes
The incubation period is from 3 to 20 days. The disease can occur in mild, moderate and severe forms. The process begins acutely, the body temperature rises to 39-40 C. The duration of the temperature reaction is 2-3 weeks. The temperature drop occurs in the form of a shortened lysis. As the temperature rises, signs of intoxication appear. Characteristic signs of leptospirosis are the occurrence of severe pain in the calf muscles and lumbar muscles, as well as polymorphic skin rash, in some patients with hemorrhages. Symptoms of increased vascular fragility are noted. During this period, the liver and spleen enlarge. Jaundice usually occurs early, sometimes from the 3rd-6th day of the disease. In severe leptospirosis, neurological symptoms are observed - phenomena of meningism or serous meningitis. Complications of leptospirosis include pneumonia, often endo- and myocarditis, polyneuritis, serous meningitis or encephalomyelitis, and eye damage.
Eye lesions occur both in the early and late periods of the disease, but there are no specific eye symptoms. Early eye manifestations of leptospirosis include, first of all, catarrhal conjunctivitis, which is usually observed during fever. It is observed quite often - in 60% of cases. Episcleritis often develops, and sometimes ulcerative keratitis or corneal lesions resembling herpetic. From the 3rd to 6th day of the disease, yellow staining of the sclera is possible. During the period of hemorrhagic manifestations, starting from the 7th to 9th day, hemorrhages are often observed: conjunctival and subconjunctival, less often in the anterior chamber of the eye, vitreous body, retina, sub- and retroretinal paramacular hemorrhages are possible. In some cases, with meningoencephalitis, diplopia appears as a result of paresis of the oculomotor nerves. Due to severe intoxication, papillitis, neuroretinitis and retrobulbar neuritis of the optic nerve sometimes develop, and sometimes anterior exudative choroiditis, manifested by opacity of the vitreous body and delicate precipitates on the posterior surface of the cornea. Combinations of iridocyclitis and toxic neuritis of the optic nerve are also noted at later stages - 2 months or more after leptospirosis. Their duration is 2-4 weeks; the prognosis is favorable.
Inflammation of the vascular tract is the most common eye lesion in leptospirosis. It occurs in 5-44% of cases, observations indicate various forms of uveitis in leptospirosis. Intoxication and intoxication-allergic factors may be important in the development of uveitis.
At an earlier stage after leptospirosis (during the first 2 months), nongranulomatous iridocyclitis of one or both eyes develops, characterized by the appearance of small precipitates on the posterior surface of the cornea, posterior synechiae, irregular pupil shape, and diffuse opacity of the vitreous body. The disease is characterized by a short course and a favorable outcome. Much less frequently, anterior exudative choroiditis develops during the same period, which is manifested only by a small number of precipitates on the posterior surface of the cornea and slight opacity of the vitreous body. In most cases, early eye changes disappear within a few weeks without any particular consequences.
Months and even 8-12 years after leptospirosis, more severe lesions of the uveal tract occur in the form of nongranulomatous anterior uveitis or iridochoroiditis of both eyes. In this case, edema, folds of Descemet's membrane, precipitates on the posterior surface of the cornea, hyperemia of the iris, posterior synechiae and significant opacity of the vitreous body due to exudation are detected. Sometimes snow-like opacities or dense membranes and white precipitates are detected in the vitreous body; development of papillitis of the optic nerve, repeated hemorrhages in the anterior chamber of the eye, "retinal" is possible. Visual acuity is sharply reduced. The changes remain for generations and are characteristic of leptospirotic lesions. Treatment of this form of uveitis is not effective enough. Exacerbations and relapses are noted.
It is possible for leptospirosis to develop bilateral hypopyon-uveitis, which is characterized by the appearance of exudate in the anterior chamber and in the pupil area, and a sharp decrease in vision. In the puncture of the anterior chamber of the eye, predominantly lymphocytes, polynuclear leukocytes, and reticuloendothelial cells are found. These forms of uveitis can be combined with serous meningitis or encephalomyelitis.
Thus, the most typical eye complications are:
- nongranulomatous iridocyclitis with a favorable course;
- anterior exudative, rapidly progressing choroiditis with a tendency towards complete resolution and restoration of vision;
- severe iridochoroiditis with persistent opacity of the vitreous body;
- optic neuritis.
The course of eye diseases in leptospirosis can be long, but the prognosis is favorable in most cases. Only in 4.5% of cases is complicated cataracts developed, and in 1.8% - partial atrophy of the optic nerves. They are mainly the cause of significant vision loss and blindness.
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Diagnosis of leptospirosis of the eyes
Diagnosis of leptospirosis eye lesions is carried out taking into account epidemiological data and the features of the clinical picture of the disease. Laboratory tests are necessary, especially if the eye pathology develops late after leptospirosis. Neutrophilic leukocytosis and increased ESR are noted in the peripheral blood with leptospirosis. The most reliable detection of leptospira is in the blood, cerebrospinal fluid, urine, and in the chamber moisture of the eye. Blood is taken twice in the acute period of the disease with an interval of 5-7 days. Serological reactions for the detection of antibodies in the blood serum are highly specific: agglutination, lysis and complement fixation, as well as the reaction of microagglutination of the moisture of the anterior chamber of the eye. A positive diagnostic titer of agglutinin of 1: 100 and higher (up to 1: 100,000) appears in the 2nd week. Its increase with the course of the disease is taken into account, which confirms the diagnosis of leptospirosis. RSK is carried out according to the generally accepted method. Diagnostic titers are serum dilutions of 1:50 - 1: 100. Specific antibodies are detected in those who have recovered for several years. Of relative value is a biological test - infection of laboratory animals by intraperitoneal, subcutaneous, or anterior chamber injection of material containing leptospirosis (blood, cerebrospinal fluid, urine, chamber moisture). Laboratory diagnostics of leptospirosis is carried out in the departments of especially dangerous infections of republican, regional, and provincial sanitary and epidemiological stations.
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Treatment of leptospirosis of the eyes
Treatment of leptospirosis eye lesions is primarily reduced to the treatment of leptospirosis. Patients are hospitalized in the infectious diseases department, where appropriate therapy is administered. First of all, antileptospirosis gamma globulin is administered intramuscularly for 3-4 days at 5-10 ml. Antibiotics are used (penicillin, chloramphenicol or ceporin, tetracycline antibiotics). Detoxification drugs are also indicated: hemodez, polyglucin, rheopolyglucin, 5-10% glucose solution are administered intravenously. In severe cases, prednisolone is used (up to 40 mg per day). Ascorbic acid, cocarboxylase, and B vitamins are widely prescribed in normal doses. Angioprotectors and hyposensitizing agents (suprastin, pipolfen, diphenhydramine, calcium gluconate) are indicated. In case of eye damage, symptomatic treatment is also carried out (local mydriatics, corticosteroids, in chronic forms pyrogenic substances, resorbing agents). Treatment of patients with late complications of leptospirosis is carried out in ophthalmological institutions.
Prevention of ocular leptospirosis
Prevention comes down to general measures, including the fight against leptospira carriers, disinfection, and active immunization of people in areas where outbreaks of the disease occur. Early diagnosis of leptospirosis and timely comprehensive treatment are necessary (order