herpes simplex scleritis

Introduction

Introduction to herpes simplex virus scleritis Herpes simplex virus (HSV) infection can cause scleritis or scleral inflammation. Straight epilepsy is caused by direct invasion of the virus during active HSV infection; scleritis is a direct invasion of the virus by active HSV or the first virus Several days after infection, it is caused by an immune response produced by the virus. Primary HSV infection occurs between 6 months and 5 years after birth, and approximately 75% of adults aged 15 to 25 are infected with HSV and produce antibodies, up to 97% over 60 years of age. basic knowledge The proportion of illness: 0.02% Susceptible people: no specific people Mode of infection: non-infectious Complications: cataract

Cause

Causes of herpes simplex virus scleritis

(1) Causes of the disease

HSV is ubiquitous. It was described in ancient Greece as it was related to human infection. In 1968, the biological characteristics and antigens between HSV-1 and HSV-2 were identified. Nahimas et al proposed HSV-1 and non-reproductive systems. Infection, HSV-2 is associated with reproductive system infection. The main body of the virus is a 25-sided symmetrical arrangement. The core of the virus is double-stranded DNA. The molecular weight is 100×106 Da. The DNA core encoding at least 70 polypeptides and the diameter of 100-110 nm is capsid protein. Wrap, protect the virus nucleic acid from nuclease damage, close to the capsid is the capsule, composed of amorphous material, wrapped in the outer shell and the membrane is a loose double-layer lipid membrane containing polyamino acids, lipids and glycoproteins Glycoprotein determines the distinguishing nature of the virus and provides a unique antigen that the host produces to respond, allowing the body to produce corresponding antibodies and sensitized lymphocytes. The viral core and capsid proteins replicate in the infection, and the replicated progeny virus only has intact virus particles. It is infectious. The primary HSV infection occurs from 6 months to 5 years after birth. About 75% of adults aged 15 to 25 are infected with HSV and produce antibodies. 97% of those over 60 years old, only 1% to 6%. Suffering After the first clinical manifestations of infection, most were subclinical, about 95% of the clinical manifestations associated with HSV infection is recurrent, and for a long time to appear after the initial infection.

(two) pathogenesis

For the first time, HSV is infected by direct contact with susceptible individuals. The virus infects peripheral marginal organs such as skin and mucous membranes, most of which are asymptomatic or recessive, and are transmitted to the local trigeminal ganglia, the superior cervical ganglion and the corneal stromal cells. (Type I) and the appendix ganglion (type II), which are carriers of life-long viruses. The latent virus can be activated by various stimuli at any time (such as fever, trauma, mental stress, ultraviolet radiation, menstruation, gastrointestinal dysfunction, Surgery and drugs, etc., and enter the replication cycle, the virus reaches the peripheral limbs through the neural network, leading to HSV recurrence, immunosuppressed individuals such as leukemia, malignant tumors or organ transplant patients, HSV recurrence is more common, and more serious.

The clinical manifestations and frequency of recurrence are related to the type of virus that is first infected (viral group genes). Only in extreme cases (leukemia, malignant tumors) can cause disease, while others have more toxic viruses in the body, which can cause serious clinical Performance and frequent recurrence, viral genes and various stimuli are important factors in causing viral activity and clinical disease.

Prevention

Herpes simplex virus scleritis prevention

Develop good hygiene practices. Do not rub your hands, towels, handkerchiefs should be washed and dried, nurseries, schools, factories and other collective units should be divided into basins or running water to wash the face, patients with herpes simplex scleritis should be actively treated, strengthen the hairdressing room, bathroom, Sanitary management of hotels and other service industries, strict disinfection systems such as towels and washbasins, and attention to water source cleaning

Complication

Herpes simplex virus scleritis complications Complications cataract

This disease can cause a variety of keratitis or keratitis, cataract, uveitis, glaucoma and scleral thinning (defect) for patients with keratitis, corneal lesions, cataract, there may be a sharp decline in vision, when less than 0.4 patients IOL should be considered for replacement. At the same time, the infection of the sclera can cause herpes zoster infection around the eyes, and patients often have severe eye pain.

Symptom

Herpes simplex virus scleritis symptoms Common symptoms Scleral vesicle marginal ulcerative keratitis Scleral perforation Tears premalignant lymphadenopathy Herpes

The first HSV infection was acute follicular conjunctivitis with pre-auricular lymphadenopathy, orbital herpes-like skin abnormalities, ulcerative orbital inflammation, about 2/3 of patients with punctate or dendritic keratitis, and a small number of patients with matrix Keratitis or anterior uveitis.

Recurrent HSV infection is characterized by keratitis including epithelial keratitis (dendritic, map-like, intermediate herpetic keratitis), stromal keratitis (necrotic, interstitial or discoid keratitis, immune ring and limbus) Vasculitis) and endotheliitis, dendritic or map keratitis caused by direct invasion of the virus; necrotizing stromal keratitis can be caused by direct invasion of the virus and allergic reactions of immune complexes; interstitial stromal keratitis, immune ring , marginal vasculitis and marginal ulcerative keratitis caused by allergic reactions of immune complexes; discoid keratitis is caused by delayed immune response; endotheliitis may be caused by direct invasion of the virus or immune response; central herpes keratitis Inflammation caused by nutritional factors, corneal stroma involvement showed endothelial gray-white KP, posterior elastic layer wrinkles, matrix edema, necrotizing, interstitial keratitis cases in the anterior chamber may have grayish white and dilute pus, corneal sensation .

Scleritis

Scleritis accounts for approximately 1.16% of patients infected with HSV, direct invasion of HSV (often accompanied by epithelial infectious keratitis or necrotizing stromal keratitis) or host immune response to the virus (with necrotic or interstitial matrix Keratitis, marginal vasculitis, discoid keratitis, marginal ulcerative keratitis) leading to scleritis, scleritis is mostly diffuse or nodular anterior scleritis, caused by immune response, the most common is necrotic Scleritis.

The main symptoms are: red eyes, photophobia, tearing, mucous secretion of conjunctival sac, severe eye pain and varying degrees of visual loss.

Signs: diffuse hyperplasia of the sclera of diffuse anterior scleritis, edema of superficial sclera, edema of the conjunctiva, inflammation easily spread, most cases of inflammation involving part of the anterior sclera, a small part of the lesion involving the entire sclera, nodular anterior scleritis The sclera is dark red and congested. The surface of the sclera is incapable of movement. The purple-red nodular bulge of hard and tender tenderness is common. A single nodule is more common. A few have nodules, which may be accompanied by scleral inflammation. If the lesion continues to develop, The formation of necrotizing anterior scleritis, which is highly destructive, causes visual impairment, early manifestations of local scleritis plaque, and acute hyperemia. The inflammatory response around the lesion is heavier than the center, and then there is no blood vessel on the scleral surface lesions and surrounding. Area, the affected sclera can be carrion-like necrosis, and spread from the original lesion, can spread the entire anterior sclera, if not treated in time, the scleral necrosis area falls off, forming scleral perforation or scleral staphyloma.

2. Scleral outer inflammation

Scleral outer inflammation is rare in HSV infection, simple or nodular, with local lymphocytic infiltration, manifested as yellow spots or dendritic keratitis of the conjunctiva or superficial sclera, the outer sclera inflammation is caused by direct invasion of the virus, a few Healed after the week, no sequelae, recurrence is rare.

Examine

Herpes simplex virus scleritis

Corneal epithelial scraping with Giemsa staining, Papanicolaou staining, can show the characteristics of HSV infection such as eosinophils, balloon-like changes, multinucleated giant cells and monocyte infiltration, but can not distinguish between HSV and VZV, with follicular Conjunctivitis, dendritic keratitis, by fluorescent staining of the upper edge conjunctiva and skin vesicles or skin, cornea, superficial sclera, scleral biopsy, can be found HSV-1, fresh dendritic, map-like corneal ulcer tissue virus More than 50% of the cases showed positive after separation. The new serological method can distinguish the first or recurrent HSV infection, because only the first infection shows an increase in HSV antibody titer, the acute phase titer is very low, and the titer is significantly increased after 4 to 6 weeks. Because most adults have anti-HSV antibodies, they are asymptomatic or subclinical.

Histopathological examination of conjunctival and scleral biopsy revealed granulomatous inflammation with epithelial cells and multinucleated giant cells and microvascular inflammatory lesions.

Diagnosis

Diagnosis and identification of herpes simplex virus scleritis

The clinical diagnosis of HSS can be established according to the characteristics of clinical manifestations, the occurrence of certain factors, and the risk of recurrent episodes. The diagnosis of HSV eye infection requires the isolation of the virus through the laboratory, but it is difficult.

Sometimes the lesions are banded and need to be differentiated from herpes zoster. The identification depends mainly on the results of laboratory tests.

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