Viral conjunctivitis is a common infection, the extent of which varies according to individual immune status and virulence of the virus, and is usually self-limiting. The clinical course is divided into two groups: acute and chronic, with the former being more common and including epidemic keratoconjunctivitis, epidemic hemorrhagic conjunctivitis, pharyngeal conjunctival fever, herpes simplex virus conjunctivitis and Newcastle fever conjunctivitis. Chronic viral conjunctivitis including infectious molluscum contagiosum blepharoconjunctivitis, varicella-herpes zoster blepharoconjunctivitis, measles keratoconjunctivitis.
I. Adenoviral keratoconjunctivitis Adenoviral keratoconjunctivitis is an important? s viral conjunctivitis, mainly manifested as acute follicular conjunctivitis, often combined with keratoconjunctival lesions. The disease is highly contagious and can occur sporadically or epidemically. Adenovirus is a deoxyribonucleic acid (DNA) virus that can be classified into 37 serotypes. Types 2, 3, 4, 7, 8, 9, 14, 16, 19, 29, 31 and 37 have been isolated from foci of ocular infection. In vitro culture of the virus requires the use of inoculated cells such as human embryonic kidney cells, which can be typed by fluorescent antibodies, complement-fixing antibody assays, neutralization assays or blood cell agglutination inhibition assays. Viral conjunctivitis caused by different types of adenovirus can have different clinical manifestations, and the same clinical manifestations can be caused by several different serotypes of adenovirus. Adenoviral keratoconjunctivitis manifests itself in two main types, namely epidemic keratoconjunctivitis and pharyngeal conjunctival fever.
Epidemic keratoconjunctivitis is a highly contagious contact infection caused by adenovirus types 8, 19, 29 and 37 (human adenovirus subgroup D). The incubation period is 5 to 7 days.
Clinical manifestations: rapid onset, severe symptoms, and bilateral eye onset. The main symptoms are congestion, pain, photophobia, and aqueous discharge. In the early stages of the disease, one eye is often affected first, and the contralateral eye is also involved a few days later, but the disease is relatively mild. In the acute phase, the eyelid is edematous and the conjunctiva is congested and edematous, with follicular and subconjunctival hemorrhages appearing within 48 hours. The formation of pseudomembranes (and sometimes true membranes) can lead to flattened scarring and lid adhesions. A few days after onset, the cornea may show diffuse patchy epithelial damage that fuses into a larger, rough epithelial infiltrate 7 to 10 days after onset. 2 weeks later, it develops into a localized subepithelial infiltrate that spreads mainly to the central cornea, with normal corneal sensitivity. After 3 to 4 weeks of disease onset, the subepithelial infiltrates intensify and are essentially uniform in morphology and size, ranging from a few to dozens. The subepithelial infiltrates are caused by a delayed allergic reaction, mainly lymphocyte infiltration in the anterior elastic and anterior stromal layers, as an immune response of the body to viral antigens. This subepithelial infiltrate can last for months or even years with gradual resorption and, in rare cases, the infiltrate eventually forms a scar, causing permanent visual impairment. Conjunctival inflammation lasts up to 3 to 4 weeks. After the primary symptoms subside, the corneal clouding may disappear after several months. Patients often present with swollen and painful preauricular lymph nodes, which are more pronounced on the side of the eye where the involvement begins, and are an important differentiator from other types of conjunctivitis, which are not present in early stages of the disease or in mild cases. It is important to note that preauricular lymph node enlargement may also be present in children with blepharospasm infection. Children may have systemic symptoms such as fever, sore throat, otitis media, and diarrhea.
Diagnosis: Acute follicular conjunctivitis and subepithelial infiltration of the cornea in the late inflammatory phase are typical features of the disease. Conjunctival scrapings show a large number of mononuclear cells and an increased number of neutrophils when there is pseudomembrane formation. Viral culture, PCR testing, and serological tests may assist in the pathogenetic diagnosis.
Treatment: Measures must be taken to reduce the spread of infection. All instruments that come into contact with an infected person must be carefully cleaned and disinfected, and patients must be advised to avoid contact with eyelids and tears and to wash their hands frequently. Avoid contact between people when possible when infection is present. There is no special treatment. Local cold compresses and use of vasoconstrictors can reduce symptoms. In the acute phase, antiviral drugs such as interferon eye drops, 0.1% acyclovir, 0.15% ganciclovir, 0.1% triazolyl nucleoside, and 4% morpholine bisphosphonate can be used to inhibit viral replication once an hour. Add antibiotic therapy in case of combined bacterial infection. In case of severe membrane or pseudomembrane, epithelial or subepithelial keratitis causing loss of vision, glucocorticoid eye drops can be considered, and the frequency of glucocorticoid eye drops should be reduced to once a day or once every other day after the disease is controlled. The application should pay attention to the gradual reduction of the drug, do not suddenly stop the drug, in order to avoid relapse; in addition to pay attention to the side effects of hormones.
2, pharyngoconjunctival fever (pharyngoconjunctival fever) is a viral conjunctivitis caused by adenovirus types 3, 4 and 7, which manifests as acute follicular conjunctivitis with upper respiratory tract infection and fever, and is transmitted mainly by respiratory secretions. It is most commonly seen in children and adolescents aged 4 to 9 years. It is often prevalent in kindergartens and schools during the summer and winter months. Sporadic cases can be seen in adults.
Clinical manifestations: The prodromal symptoms are generalized malaise, rise in body temperature above 38°C, self-conscious lacrimation, red eyes and sore throat. Patient signs are ocular follicular conjunctivitis, transient superficial punctate keratitis and subepithelial clouding, and enlarged preauricular lymph nodes. Pharyngeal conjunctival fever may sometimes present with only 1 to 3 major signs. The duration of the disease is about 10 days and is self-limiting.
Diagnosis: The diagnosis can be made on the basis of clinical manifestations. A large number of mononuclear cells are seen in conjunctival scrapings and no bacterial growth in culture.
Treatment and prevention: There is no specific treatment. The treatment and preventive measures for epidemic keratoconjunctivitis can be referred to. Do not go to public places and swimming pools during the onset of the disease to reduce the chance of transmission.
Epidemic hemorrhagic conjunctivitis Epidemic hemorrhagic conjunctivitis is an outbreak of an epidemic self-limiting ocular infection caused by enterovirus type 70 (occasionally A24 coxsackievirus), also known as Apollo 11 conjunctivitis, which first broke out in Ghana in 1969 and had a widespread epidemic in China in 1971. The disease has been endemic in many countries and islands.
Clinical manifestations: short incubation period of 18-48 hours (short course of 5-7 days), common symptoms include eye pain, photophobia, foreign body sensation, lacrimation, subconjunctival hemorrhage, and eyelid edema. Subconjunctival hemorrhage is flaky or punctate, starting from the superior bulbar conjunctiva and spreading to the inferior bulbar conjunctiva. Most patients have follicular formation with epithelial keratitis and enlarged preauricular lymph nodes. Anterior uveitis occurs in a minority of patients, and some patients also have systemic symptoms such as fever and muscle pain. India and Japan have reported isolated cases of polio-like lower limb dyskinesia.
Diagnosis: Symptoms of acute follicular conjunctivitis, along with significant subconjunctival hemorrhage and enlarged preauricular lymph nodes, are the basis for diagnosis.
Treatment and prevention: There is no specific treatment, it is self-limiting. Strengthening personal hygiene and hospital management to prevent transmission is the key to prevention.