Pediatric viral stomatitis

Introduction to pediatric viral infective stomatitis The most common incidence of herpestics stomatitis (herpeticstomatitis) is an oral mucosal disease caused by herpes virus infection, which may also occur in the lips and perioral skin. Self-limiting. basic knowledge The proportion of illness: 23% Susceptible people: young children Mode of infection: droplet spread Complications: convulsions in children

Pediatric virus infectious stomatitis etiology

(1) Causes of the disease

Herpetic stomatitis, also known as herpes gingivitis, is an acute oral mucosal infection caused by herpesvirus type I. It can be caused by droplets and contact infections, febrile diseases, colds, digestive disorders, and excessive fatigue.

(two) pathogenesis

Herpes simplex virus belongs to DNA virus. Human herpes simplex virus can be divided into two types, namely herpes simplex virus type I and herpes simplex virus type II. Type I mainly causes infection of skin, mucous membranes and organs other than genitals; type II mainly causes The skin mucosa of the genital area and the infection of newborn babies, type I and type II viruses can be identified by fluorescence immunoassay and cell culture. There is cross-immunization between the two. In recent years, studies have found that herpes simplex virus type I and type II are associated with lip cancer and Cervical cancer is related.

Human is the natural host of herpes simplex virus. About half of the normal people are carriers of the virus. The virus enters the human body through the respiratory tract, oral mucosa or damaged skin. The primary infection is mostly obtained by direct contact with the patient, such as by kissing. Tableware used in patients with herpetic gingivitis, etc., normal herpes simplex virus infection is mostly confined to the surface of the skin mucosa, especially susceptible, such as newborns, severe malnutrition or other infected children, immunodeficiency and application of immunity Inhibitors, hematogenous dissemination can occur, primary infections are mostly recessive, only 10% of patients have clinical symptoms, after the primary infection, the virus can continue to lurk in the body, because herpes simplex virus does not in the human body Produces permanent immunity, so whenever the body's disease resistance is weakened, such as fever, gastrointestinal dysfunction, menstruation, pregnancy, infection, excessive fatigue and emotional environment changes, the virus in the body is active and causes disease.

In the early stage of primary infection, complement-dependent neutralizing antibodies are present, that is, complementation is required to neutralize the virus, and in the latter stage, non-complement-dependent neutralizing antibodies are used. Antibodies play a role in eliminating viremia and shortening the course of disease, but not To prevent recurrence of infection, some susceptible people may still have serious diseases despite antibodies. This may be due to the virus being lurking in white blood cells, or the virus is still infective with antibodies, and immune lymphocytes, interferons or secretory antibodies. Relatively lacking, serum-positive patients have delayed-type allergic reactions to herpes simplex virus antigens, and their sensitized T lymphocytes can release various lymphokines, and are cytotoxic to target cells infected with herpes simplex virus, which can directly kill, therefore, Patients with cellular immunodeficiency and long-term use of immunosuppressive agents may have severe or prolonged herpes simplex virus infection. Macrophages also have a role in limiting herpes simplex virus replication and preventing its spread. Sexual immunity can eliminate most of the virus, a small number of viruses invade the peripheral nerves, and along the nerves The axonal migration to the trigeminal ganglion or sensory ganglion, latent in the nerve cells, the latent mechanism remains unclear, and some believe that it is related to the following factors:

1. Since the nerve cells do not proliferate and lack the specific transcriptase required for viral replication, both the virus and the host cells remain intact.

2. The specific IgG antibody binds to the viral surface antigen, so that the viral genome is in a state of inhibition, and thus lurks for a long time. When there is fever, cold, wind, sun, trauma, menstruation, pregnancy and anxiety, the surface charge of the nerve cells The change can weaken or shedding the antibody to the virus, the viral genome is de-suppressed, reactivated, and migrates along the axons to the epithelium near the nerve endings. If the cellular immunity is also inhibited, the virus multiplies and causes herpes.

Pediatric virus infectious stomatitis prevention

Do a good job in pregnancy, promote breastfeeding, improve the environment, avoid or reduce pollution, avoid passive smoking, frequent outdoor activities and sun exposure, timely increase or decrease clothes during climate change, regular ventilation in the living room, keep indoor air fresh, have respiratory tract When infectious diseases are prevalent, indoors can be irradiated with ultraviolet rays or fumigation with lactic acid, vinegar, Chinese medicine Atractylodes, etc., isolated from patients, not in crowded public places, strengthen nutrition, and give high protein diet (4g/kg per day, 3g for infants) /kg, children 2.5g/kg) and foods rich in vitamins.

Pediatric viral infectious stomatitis complications Complications

Patients with severe systemic symptoms may cause convulsions due to high fever, or secondary bacterial infections may prolong the course of the disease.

Pediatric virus infectious inflammatory symptoms common symptoms antifeeding herpes high fever stomatitis edema blush congestion

2 to 3 days before the onset of herpes (latency), children often have irritability, refusal to eat, fever and local lymphadenopathy, body temperature decreased after 2 to 3 days, but oral symptoms increased, the lesion initially showed diffuse mucosal flushing, at 24h The tip-sized blister gradually appears in a densely integrated group, which is round or elliptical, surrounded by red blush, and the blister is quickly ruptured, exposing superficial ulcers or ulcers to form a large ulcer, and the surface is covered with yellowish white secretions. The disease is self-limiting, the oral mucosa returns to normal within 1 to 2 weeks, no scars are left after the ulcer is healed, and the blister cells, virus isolation and serological tests can help diagnose.

Pediatric virus infectious stomatitis examination

1. routine inspection

Generally normal, a small number of peripheral blood leukocytes may increase.

2. Cytological examination

Skin mucosal herpes scrapings were taken for smear to examine multinucleated giant cells and nuclear eosinophilic inclusion bodies.

3. Virus culture

Herpes simplex virus isolation and culture is more successful, many tissue culture methods can be applied, it is advisable to take fresh blister inoculation.

4. Determination of serum antibodies

Neutralization, complement fixation or indirect immunofluorescence assays have multiple antibodies in the patient's serum.

5. Histopathological changes

The recurrence is the same as the pathological changes of the primary infection. The cell degeneration and necrosis are dominant. The epidermal cells undergo balloon degeneration, reticular degeneration and coagulative necrosis. The epidermis is loosened to form blisters. The balloon degeneration is more obvious and occurs in the blister. Bottom, so vesicles are often single-atrial, vesicles in the epidermis can eventually develop into epidermis blister, a few reticular degeneration can be seen in the blister wall, sometimes visible nuclear division and epithelial multinucleated giant cells, red blood cells and neutral granules in the old vesicles In the cells, the intranuclear inclusion bodies were observed in the invaded cells. The inclusion bodies were basophilic in the early stage, and Feulgen was positive, but in the later stage, it became eosinophilic and Feulgen was negative.

Generally, no special examination is needed. If necessary, the child with convulsions can do EEG and other examinations.

Diagnosis and identification of pediatric viral infectious stomatitis

diagnosis

1. Children who are more common in children aged 1 to 5 can also be seen in adolescents. There is a history of high fever before onset.

2. Individual or clustered herpes in the oral mucosa, congestion and edema of the gingival margin and attachment, and herpes on the perioral skin and nose.

3. Take the skin mucosa herpes scraping as a smear, check the multinucleated giant cells and intranuclear eosinophilic inclusions, which will help diagnose.

Differential diagnosis

Stomatitis

Most of the patients are adults, with a history of recurrent oral ulcers, ulcers 10 to 30 or more, scattered, mostly non-fused, not clustered, occur in non-keratinized mucosa, most of the systemic response is light.

2. Multi-type exudative erythema

Polymorphic erythema is a more complicated self-limiting inflammatory skin mucosal disease, which occurs in young and middle-aged adults. It is more common in spring and autumn. The clinical manifestations are oral mucosal edema and congestion, large blisters, and blister formation. Lip damage is very common, erosive edema and scarring, often combined with underarm infection, easy bleeding, rash is pleomorphic such as papules, macules, blisters, erythema, etc., typical lesions are erythema-sized erythema, color Bright red, clear boundary, small blisters in the center.

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