Lyme disease scleritis

Introduction to Lyme disease scleritis Lymedisease is a contagious disease caused by Borrelia burgdorferi that can invade many human organs, mainly involving the skin, nervous system, joints, heart and eye tissue. basic knowledge The proportion of illness: 0.025% Susceptible people: no special people Mode of infection: bite spread Complications: keratitis conjunctivitis scleritis

Cause of Lyme disease scleritis

(1) Causes of the disease

Lyme disease is recently recognized as a vector-borne infectious disease caused by Borrelia burgdorferi. In 1982, Burgdorfer and colleagues isolated a Borrelia Burgdorferi from the Daming hard palate. The characteristics of the study are closely related to Lyme patients and appear in various specimens of patients, thus determining the ultimate cause of Lyme disease.

(two) pathogenesis

It is easy to find Borrelia pallidum in the body, but it is very difficult to find in the human body. Part of the reason is that the latter has relatively few pathogens in the body tissues and body fluids. The possible pathogenic process of Borrelia burgdorferi is based on cockroaches. Infected by the skin, after 3 to 32 days of incubation, the Borrelia burgdorferi moves outward to the skin, forming erythema chronicum migrans (ECM), which later spread to the lymph (local lymphadenopathy), or into the bloodstream. It spreads to various organs of the body (central nervous system, joints, heart, liver, spleen and eyeballs), or other parts such as skin. Mother-to-child transmission is extremely rare, although it is extremely difficult to find Borrelia in the late Lyme disease. However, in the process of Lyme disease, Borrelia burgdorferi in the liver may continue to play a role in disease.

The occurrence of Lyme disease is associated with specific immune abnormalities. In the early stage of the disease, almost all cases have evidence of the presence of circulating immune complexes (CIC). Continuous detection of serological IgM is the only and most helpful laboratory diagnosis of disease activity. According to this, in some cases, primary disseminated immune-mediated inflammatory lesions can be localized, and can also be transmitted in whole body tissues, especially joints.

In addition to the factors associated with the pathogenicity of Borrelia burgdorferi-specific isolates, the composition of immunogenetics also plays an important role in determining whether an infected person has the ability to clear his own Borrelia.

Lyme disease scleritis prevention

Eliminate the vector sputum while avoiding entry into the affected area.

Lyme disease scleritis complications Complications keratitis conjunctivitis scleritis

Eye complications include uveitis, endophthalmitis, keratitis, conjunctivitis, mumps, scleritis or sclera, and keratitis manifests as opacity of the matrix, leukoplakia or marginal ulcers.

Lyme disease scleritis symptoms common symptoms herpes herpes papules fatigue mental disorders dementia keratitis retinal hemorrhage macular cystic edema retinal detachment

1. Clinical features: For the sake of convenience, Lyme disease is divided into three clinical periods, but each period can overlap with each other, and most cases do not fully have the clinical manifestations of Phase 3.

(1) Phase I: characteristic skin ECM with clinical manifestations within 1 month after being bitten, so Lyme disease is also known as chronic migratory erythema, with red macules or papules starting with carrying The bite of the spiral body lasts for a long time. When the congestion area is enlarged to about 1.5cm, part of the middle zone is clearly visible, the outer edge of the lesion is red, the center is red and the texture is hard, and even herpes or necrosis is formed. Other manifestations are typically intermittent or variable and are important for early diagnosis of Lyme disease.

(2) Phase II: weeks to months after the start of bite, characterized by neurological symptoms (meningitis, facial paralysis, peripheral radiculitis) and heart disease (myocardial infarction, myocarditis, atrial fibrillation, paroxysmal room) Ventricular block, etc.).

(3) Phase III: The characteristic manifestations of biting after 2 years are arthritis, neurological manifestations (neuropsychiatry, fatigue syndrome, dementia, myelitis, mental disorders, ataxia, etc.).

2. Ocular manifestations: can occur in all stages of Lyme disease, but common in the second phase, including oculomotor nerve, nerve expansion, facial nerve palsy, optic neuropathy (opic neuritis and optic nerve inflammation, optic disc edema, ischemic Optic neuropathy, retinopathy (retinal hemorrhage, exudative retinal detachment, cystoid macular edema).

Examination of Lyme disease scleritis

Enzyme-linked immunosorbent assay (ELISA) and indirect immunofluorescence antibody (IFA) are the most commonly used serological tests for the diagnosis of Lyme disease, both of which measure the response to serum Borrelia in the serum. IgM, IgG, often negative at early stage, IgM specific for anti-B. burgdorferi (BB) antibody first appeared after 3 to 4 weeks of infection, peaked at 6-8 weeks, then gradually decreased, and specificity appeared 2 months after infection. IgG, and it continues to rise during the active period, can not fall for life, after effective long-term treatment, IgG decreased, but still higher than non-infected, Lyme disease serological examination found that antibodies after antibiotic treatment or patient application When the immunosuppressant is used, the reactivity is decreased. When the ELISA or IFA titer is 1:256, the clinical manifestations can be used to diagnose Lyme disease scleritis or scleral inflammation. This test has a considerable part of false positive results, mainly because of Other spirochetes have crossovers such as Treponema pallidum, and Western blot can effectively identify various false positives such as syphilis, Rocky Mountain spotted fever, autoimmune diseases, uveitis and other gods. Due to system abnormalities, it is difficult to grow Borrelia burgdorferi at the infected site, and tissue culture is more negative.

Fundus fluorescein angiography (FFA) and retinal functional tests such as electroretinogram (ERG) and visual evoked potential (VEP) can determine changes in retinal morphology and function, and clarify the extent of the lesion.

Diagnosis and diagnosis of Lyme disease scleritis

diagnosis

Scleritis and scleral inflammation may be associated with direct invasion of Borrelia burgdorferi or its metabolites, which may be characterized by recurrent diffuse anterior scleritis, optic disc edema and cystoid macular edema, and scleral inflammation in Lyme. Other ocular diseases of the disease, such as vesicular conjunctivitis, occur after stromal keratitis, which may suggest an untreated recurrent infection of Lyme disease.

Differential diagnosis

There are many similarities between scleritis and scleral inflammation caused by syphilis and Lyme disease. The identification of the two is particularly important. The syphilitic uveitis accounts for about 4% of the secondary syphilis, but it can also occur inappropriately. In some patients in the first or third phase of treatment, keratitis and iritis in syphilis patients are the most common manifestations. The main difference between syphilitic keratitis and Lyme disease keratitis is that there is a large amount of syphilitic keratitis in the early stage. New blood vessels are formed, and patients with Lyme disease do not have VDRL-positive results.

ECM is a unique early lesion of Lyme disease. When typical ECM occurs, almost no other lesions can be confused with it. However, in some cases, ECM is not found, while in other patients, the appearance of ECM is not completely characteristic. Sexual lesions are erythema multiforme, but blisters, mucosal lesions, and palm and plantar involvement are not characteristic features of Lyme disease. The cheek rash may suggest systemic lupus erythematosus, urticaria-like rash, serum disease, etc. .

Early flu-like symptoms may be misdiagnosed, especially if there is no ECM, and this erythema is not the earliest signs. Severe headache and neck stiffness may be aseptic meningitis, abdominal lesion syndrome, systemic tenderness. Lymphadenopathy and infectious mononucleosis.

Late Lyme disease is similar to other immune-mediated diseases. Like rheumatic fever, Lyme disease can be accompanied by sore throat, followed by migratory polyarthritis and carditis, but no evidence of heart valve involvement, no previous chain History of cocci infection, local facial paralysis is similar to Bell palsy caused by other causes, children with Lyme disease scleritis and arthritis, the performance is the same as adolescent rheumatoid arthritis without joint morphological changes, the only difference is The former does not have anterior uveitis.

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