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Common Viral Skin Diseases in Children – Measles, Hand, Foot and Mouth Disease and Exanthema Subitum


Measles, children’s acute rash and hand, foot and mouth disease are common viral skin diseases, which are often caused by children, but not only for children, but also for adolescents and adults. The main treatment is antiviral, supportive therapy and symptomatic treatment. Clinically, these viral skin diseases have some atypical symptoms in addition to typical symptoms, especially for some young children, which often lead to misdiagnosis and mistreatment.

  1. measles,rubeola morbilli

Measles is a highly contagious acute infectious disease caused by measles virus, which is characterized by fever, conjunctivitis, upper respiratory tract inflammation, oral mucosal plaque (Koplik’s plaque) and whole body red maculopapular rash. Before the advent of measles vaccine, except for the protection of maternal antibodies in the short period of neonatal, everyone is susceptible and the mortality rate is high. Even with the use of measles vaccine, more than 100,000 patients die every year worldwide, and in some developing countries even more than 5%. Since the application of the vaccine, the susceptible person has a complicated performance, and the incidence of adolescents and adults has increased. In addition, the proportion of infants under 8 months of age has increased due to the difference in immunity obtained from artificial infection with measles. Most of the clinical symptoms and signs of measles, rash time, sequence and rash shape are very typical, but the clinical manifestations of some patients are not typical, showing “heterotypic” measles, such as hemorrhagic measles, herpes simplex. Serious complications such as bronchial pneumonia, acute heart failure, encephalitis, laryngitis, etc. are significantly reduced.

1.1 Typical measles

Almost all of the vaccination failures and unvaccinated infections are typical measles, and about 1 in 6 of the secondary immunocompromised infections also show typical measles. The course of the disease can be divided into three phases.

1.1.1 Precursor period

The prodromal period is generally 3 to 4 days. Mainly manifested as upper respiratory tract inflammation and conjunctival inflammation, fever, cough, sneezing, salivation, tearing, photophobia, conjunctival hyperemia, pharyngeal congestion, etc., and abdominal pain, diarrhea. Two to three days after onset, about 90% of patients had measles mucosal plaques on the buccal mucosa of the first molar on both sides of the mouth, which is Kop-lik’s plaque, which is an important basis for early diagnosis.

1.1.2 Rash period

The rash period is 3 to 5 days. Generally, on the third to fourth days of fever, a rash begins to appear when respiratory symptoms and body temperature peak. The order of rash is: behind the ear, hairline, forehead, face, neck, and gradually extend to the trunk, limbs, and finally reach the palm and sole of the foot, reaching a peak at 2 to 5 days. The rash began as a pale red maculopapular rash, with a diameter of 2 to 4 mm, scattered and gradually increased, showing a bright red color. Later, it gradually merged into a dark red, irregular shape or small patchy maculopapular rash, and the skin between the rash was normal. The rash is congestive and the color fades. When the rash occurs, the systemic symptoms are aggravated, the body temperature can be as high as 40 °C, conjunctival congestion, photophobia, lethargy, and sometimes paralysis. At the same time, respiratory symptoms are aggravated, coughing is frequent, pharyngeal redness and pain, hoarseness, swollen lymph nodes in the neck, redness and swelling of the tongue, sometimes resembling a scarlet hot bayberry tongue, and the spleen may be slightly enlarged. This stage of the lungs often has dry and wet voices.

1.1.3 Recovery period

The recovery period was about 10 to 14 days. After the rash reached 3 to 5 days, the body temperature began to decrease, and it decreased to normal within 12 to 24 hours. The systemic condition improved rapidly, and the rash began to subside. The order of regression was the same as the order of rash. After the rash retreats, there is a light brown pigmentation, mainly torso, which disappears in about 1 to 2 weeks, and has diagnostic value for the measles recovery period. The rash subsided for about 2 weeks, and the sputum was finely visible.

1.2 Special type of measles

1.2.1 Light measles

Most of them are caused by the body’s immunity to measles virus, such as infants under 6 months, recently injected immunoglobulins, past measles vaccine or second measles. After infection, the clinical symptoms are mild, such as fever and upper respiratory tract symptoms are mild, measles mucosal plaque is not typical or does not appear, rash is sparse, the course of disease is short, less complications, but the immunity is the same as typical measles.

1.2.2 No rash measles

In patients with low immunity, such as leukemia, malignant tumors, congenital immunity, or immunosuppressive agents, they can also be seen in passive immunization during the incubation period; some vaccination against measles vaccine within 6 months to half a year, re-contact Measles patients may also develop symptoms when they are vaccinated against measles. Patients may present with fever, respiratory catarrhal symptoms, atypical mucosal plaques, but no rash. If the patient has serious complications such as acute encephalitis, it will be very difficult to diagnose, and must be based on epidemiology and laboratory tests. diagnosis.

1.2.3 Severe measles

This type is more common in children with malnutrition, low immunity or defects, or children with other diseases, or patients with secondary bacterial infections, or patients with frequent measles. The onset is rapid, the patient has high fever or super high fever, convulsions, long heat stroke, repeated convulsions, shortness of breath, cyanotic purpura, rapid pulse, severe symptoms of poisoning, severe rash, densely integrated tablets, dark red and fused into pieces ( Toxic measles). Sometimes hemorrhagic rash is seen, accompanied by visceral hemorrhage (hemorrhagic measles); sometimes measles is herpes-like, can be fused into a bullous (herpes measles); sometimes the rash suddenly retreats or the rash is not transparent, leaving a few blue-purple rashes, complexion Pale or blue-gray, severe systemic and respiratory symptoms, increased heart rate, coldness at the end of the extremities, mostly due to cardiac insufficiency or circulatory failure (shock measles). These patients are often critically ill and have a high mortality rate.

1.2.4 Atypical measles syn-drome

Also known as atypical measles, refers to the past inactivated measles vaccine, after a few months or years after the measles antibody level decreased significantly, and then infected with measles virus or re-injection of inactivated measles vaccine caused by the disease, mostly occurred in 10 ~ 24-year-old young people are not contagious. The pathogenesis of this disease is not fully understood. Most of them believe that this line is caused by delayed hypersensitivity reaction to measles virus. The clinical symptoms, rash appearance order and lung lesions are different from typical measles. The characteristics of such measles are: atypical symptoms in the prodromal period, such as fever, upper respiratory tract catarrhal symptoms, no more Koplik’s plaques; rash sequence begins at the distal extremities, gradually close to the extremities, trunk and face; rash and Common type can be small, punctate, herpes, purpura or wheal, pleomorphic; often complicated by pneumonia, pleural effusion, lung shadow can last for several months to 1 to 2 years, and other complications Rare, the prognosis is better. The diagnosis was based on a rise in measles antibodies during the recovery period, but the measles virus could not be isolated.

1.2.5 Neonatal measles

If there is no measles antibody or antibody level in the newborn mother, the newborn fails to obtain sufficient protective antibodies from the mother. At this time, the newborn has not reached the planned immunization measles vaccination age and failed to actively immunize. Newborn measles can easily occur if the mother is infected with measles before or during the first few days of delivery, or if the child is in close contact with measles. Most children with typical measles, fever, upper respiratory tract inflammation, conjunctivitis and dense rash, often complicated by pneumonia, need to be treated with antiviral, antibiotics, if necessary, immunoglobulin treatment.

1.2.6 Congenital measles

If the pregnant mother suffers from measles before labor, the measles virus can pass through the placental barrier, which can cause intrauterine infection and cause congenital measles in newborns. The child is born with diffuse measles-like erythema on the skin, easy to develop pneumonia and skin infections, and can be treated with intravenous immunoglobulin. In the process of measles, due to high fever and loss of appetite, the nutritional status of children may be deteriorated, vitamin A deficiency may occur, corneal opacity and softening may occur, and development is extremely rapid. Finally, blindness may be added. Vitamin A supplementation may prevent children with congenital severe measles. The occurrence of complications.

1.2.7 Pregnancy measles

Infected with measles in the first trimester, the virus affects the nervous system and can increase the early and late abortion rate. In the middle and late pregnancy, measles is easy to cause stillbirth and premature birth. Pregnant women with measles near the birth can pass measles to the fetus through the placenta, causing measles to occur in the newborn. .

1.3 Complication

1.3.1 Pneumonia

Pneumonia secondary to bacterial or other viral infections is the most common complication of measles, and even serious respiratory complications such as pneumothorax, emphysema, pulmonary failure or acute respiratory distress syndrome are the main causes of measles death, mostly in A rash period.

1.3.2 Laryngitis

Mild laryngitis in the course of measles is one of the symptoms of measles and has a good prognosis. Secondary laryngitis is caused by Staphylococcus aureus or hemolytic streptococcus, and severe cases can be caused by asphyxia caused by sore throat obstruction.

1.3.3 Heart dysfunction

More common in children under 2 years of age, due to measles viremia, or complicated by pneumonia, high fever, hypoxia, dehydration and other causes of cardiac insufficiency. A small number of patients have myocarditis or pericarditis.

1.3.4 Liver damage

In recent years, measles comorbidities, liver damage cases have increased significantly, more common in adult patients, the incidence rate of 31% to 86%. Liver damage is more common in the acute phase of measles, that is, on the 5th to 10th day of the disease course, most of the liver function returns to normal within 2 to 4 weeks, and individual patients can last for about half a year.

1.3.5 Encephalitis

Encephalitis refers to inflammation of the brain parenchyma. Typical symptoms are fever, headache, and altered consciousness. Other symptoms include disorientation, behavioral abnormalities, speech disorder, hemiplegia, and epilepsy. It is the most common neurological complication of measles. The symptoms of measles encephalitis are mostly non-specific, so they are often misdiagnosed clinically. Vaccination can significantly reduce its incidence, treatment is mainly symptomatic and supportive therapy. Measles encephalitis includes the following four types. Primary measles encephalitis

The incidence rate is about 1 ‰ to 2 ‰. Primary measles encephalitis usually occurs in the rash stage, and its pathogenesis is still unclear. At present, it is considered to be the primary invasion of nerve cells by the virus, followed by chemokine induction and lymphocyte infiltration, and can be found in cerebrospinal fluid. The detection of measles virus RNA also tends to support this theory. The main treatment is supportive therapy, the mortality rate is about 10% to 15%, and 25% is permanent nerve damage. Acute disseminated encephalomyelitis

The encephalitis is caused by immune factors, and the incidence of measles is about 1‰, which can also occur after vaccination with measles, about 1 to 2 /ppm. Acute disseminated encephalomyelitis is the most common central system complication of measles virus infection. It usually occurs on the 2nd to 30th day after infection, and it is often difficult to distinguish it from primary measles encephalitis. Its pathogenesis is mainly molecular simulation, circulating antibodies act on myelin proteins, causing central nervous system dysfunction, including visual impairment, dysuria and reduced reflexes. One-third of patients will relapse and develop an increased risk of multiple sclerosis. The main treatment is glucocorticoids and intravenous immunoglobulins, with a child mortality rate of about 5% and an adult mortality rate of about 25%. Measles inclusion body encephalitis

The encephalitis mainly occurs in immunodeficient children, usually occurring within 1 year after measles infection or vaccination, mainly manifested as mental disorders, dyskinesia and epilepsy. The measles virus persists due to impaired T lymphocyte function in the child, but the measles-like rash mediated by T lymphocytes does not appear or is mild. At the beginning, cerebrospinal fluid examination is generally normal, or there is a small increase in cells and protein. As the disease progresses, measles-specific antibodies in cerebrospinal fluid gradually increase. At autopsy, measles virus RNA was detected in brain cells. Treatment is mainly supportive therapy, and ribavirin may be effective. The mortality rate is approximately 75%. Subacute sclerosingpanencephalitis,SSPE

A chronic lethal brain degenerative disease caused by a defective measles virus that continuously infects the central nervous system. Mutations in the measles virus M gene are important causes of persistent infection. The incidence is about 1 /25,000, but the incidence of young children may be higher. The pathogenesis is due to the inability of the body to completely eliminate the virus during acute infection. In the first two years, the virus mutated, resulting in persistent infection and progressive deterioration. The patient’s neurological symptoms usually appear 6 to 15 years after the measles virus infection, and the pathogenesis is still unclear. The characteristic pathological manifestation is intranuclear inclusion bodies. Early clinical manifestations of mental decline and mood changes, characteristic rhythmic myoclonus soon appeared, EEG showed periodic complex waves, increased IgG in cerebrospinal fluid, elevated levels of anti- measles antibodies in serum and cerebrospinal fluid, and almost advanced cerebral cortex function Completely lost. The disease is progressive, and patients generally die from circulatory failure or secondary infection 1 to 3 years after onset, with a mortality rate of almost 100%. There is currently no effective and long-lasting treatment for this disease, mainly antiviral and symptomatic treatment. Intraventricular injection of interferon-α combined with oral isoproterenol can improve the condition.

1.3.6 Else

Due to improper care, poor diet, poor hygiene, etc., patients often have complications such as keratitis, corneal ulcer, stomatitis, otitis media, lymphadenitis, suppurative ocular membrane inflammation, enteritis, appendicitis, meningitis, etc. . Severe or fatal giant cell pneumonia can occur in children with impaired immune function.


  1. Hand-foot-mouth disease,HFMD

Hand, foot and mouth disease is a common viral infectious skin disease in children. It is mainly characterized by small blisters in the hands, feet and mouth with fever. The disease can be sporadic or erupted, and in a few cases serious complications of the heart, brain, lungs and other organs can occur. The pathogens causing the disease are mainly Coxsackievirus, Echovirus and New Enterovirus of the Genovirus family Enterovirus, Coxsackievirus 16 (CA16) and Enterovirus 71 (enterovir). -us, EV71) is the most common pathogen, followed by A6, A10, A5, A9, B2, B5, B13, and Echovirus type 11. Among them, severe cases are more common with enterovirus type 71 (EV71), and common cases are more common with coxsackievirus type A16 (CA16) and other types of viruses. In 2008, a large-scale HFMD outbreak occurred in China, with approximately 490,000 infections and 126 deaths. Since May 2008, China’s Health Planning Commission has listed HFMD as a national statutory Class C infectious disease and implemented nationwide surveillance. In 2008 and 2010, China developed guidelines for the diagnosis and treatment of hand, foot and mouth disease. In 2016, the EV71 inactivated vaccine was marketed in China and was used to prevent hand, foot and mouth disease caused by EV71 infection. It is currently the only vaccine that can be used to prevent HFMD.

2.1 Typical skin lesions of HFMD

The incubation period of HFMD is 3 to 7 days. There may be prodromal symptoms such as hypothermia, sore throat, headache, vomiting and loss of appetite before rash. Some children have no general malaise. The rash is a red rash at first, and it quickly develops into a blister of 2 to 4 mm. The blister wall is thin, the internal fluid is clear, the circumference is surrounded by redness, the oral mucosa is scattered in the herpes, and the blister is broken to form a gray-white erosion surface or a shallow ulcer surface. With pain, the child can manifest as salivation, refusal to eat, rash often occurs in the hands, feet, mouth, elbow, knee, buttocks are also good sites, but some patients are incomplete. Oral invasion rate is the highest, more than 90% of patients have oral mucosal damage, which is one of the symptoms identified with other rash diseases. Most children have mild clinical symptoms with a course of about 1 week.

2.2 Atypical skin lesions of HFMD

HFMD atypical lesions refer to no skin lesions, single site lesions or multiple site lesions (involving the limbs or the whole body), and skin lesions do not manifest as herpes. The following are mainly reported.

2.2.1 Maculopapular

Such lesions are mainly punctate rashes, rashes are small and small, and even do not form typical blisters, mainly limited to the ends of the limbs such as the hands and feet, often associated with EV71 infection, clinical conditions are heavier, some can be combined with heart, brain, lungs, etc. Damage to organs can cause death.

2.2.2 Generalized vesicular bullae

The skin lesions are widely distributed, except in the hands, feet, mouth, buttocks, etc., and can also be found in the trunk, limbs, perioral and external genitalia. The degree of skin lesions is heavy and the morphology is diverse. Common blisters or bullae are common, which are mostly related to CA6 infection. Can also be seen in other types of Coxsackie virus infection, the condition is generally mild, complication of organ complication and death are rare.

2.2.3 Beau’s line and onycho-madesis

A nail loss is a painless non-inflammatory nail damage caused by temporary growth disorder of the mother cell. It is characterized by the separation of the proximal deck from the nail matrix and the nail bed, and eventually shedding completely, often with various infections, drug reactions, malnutrition. It is related to factors such as severe systemic diseases, nail trauma, and periungual inflammation. It is the extreme form of Beau’s line. In 2000, Clementz first reported 5 children with HFMD. A diagnosis of nail damage occurred within 3 to 8 weeks after diagnosis. The fingers and nails can be affected. The performance is Beau’s line and dislocation. Afterwards, there are reports in different parts of the world. At present, it is believed that nail detachment may be a late complication of hand, foot and mouth disease, and the mechanism is still unclear. The clinical manifestation is that the proximal nail begins to become empty or white, and then separated from the nail bed, which can be single or multiple fingers and nails. Involved, it occurred more than 3 to 12 weeks after the diagnosis of HFMD. Mixed infections of CA6, CA10, EV71, CB1, CB2, CA16 or other types of enteroviruses and viruses may be the cause of nail loss. There is no special treatment for treatment, and oral multivitamins can also be given. The disease usually returns to normal after 1 to 4 months.

2.2.4 Other skin manifestations

Some children with CA6 infection may also present with sputum or purpura type lesions, mainly in the extremities, and some patients may also have Gianotti-Crosti-like appearance, desquamation and pigmentation.

2.2.5 Coxsackievirus6,CA6 infection

At present, in most countries and regions, CA16 and EV71 are still the most common pathogens of HFMD, but in recent years, HFMD caused by CA6 in the world has a clear upward trend. In 2011, Guangzhou City found that CA6 can cause typical HFMD, ranking third in the city’s HFMD pathogen; in 2013 and 2015, CA6 became the main pathogen of Beijing HFMD. Compared with the classic HFMD, the CA6-infected HFMD rash is more widely distributed. In addition to the hand and foot parts, the perioral, trunk, extremities, and perianal are often involved. The main clinical manifestations are generalized vesicular bullae, early papillary rash or polymorphous erythematous rash. With the development of the disease, it rapidly develops into blisters and even bullae after 1~2 days. The basement is flushed and partially merged into pieces with obvious pain. And itching, scarring and scaling when it subsides. Some children with multiple forms of rash such as maculopapular rash, herpes can occur at the same time, due to a wide range of distribution, more herpes, often misdiagnosed as varicella, bullous impetigo, primary bullous skin disease or herpes Eczema. A nail loss may occur in the later stages of the disease. CA6-infected HFMD lesions also tend to occur in previously traumatic or irritated areas such as sunburn, diaper dermatitis, and fungal infections. In addition, CA6 infection can also be characterized by Gianotti-Crosti-like lesion distribution, including the cheeks, buttocks and torso extension.

2.3 Severe HFMD

A small number of HFMD cases progress rapidly. Meningitis, encephalitis, meningitis, pulmonary edema, circulatory disorders, etc. occur in the first to fifth episodes of the disease. Most of them are caused by EV71 infection. Very few cases are critically ill and can cause death and survival. There are sequelae left. Most of the deaths were in children under 3 years of age. The main causes of death were brainstem encephalitis and neurogenic pulmonary edema. Risk factors for death include convulsions, difficulty breathing, cyanosis, cold extremities, and vomiting.

Currently, EV71 is the main cause of severe HFMD and death. According to statistics, the number of severe HFMD diagnosed in Chinese mainland laboratories from May 2008 to December 2011 was 27,444, and the composition ratios of EV71, CA16 and other enterovirus infections were 81.75%, 4.52% and 13.73%, respectively. In 1754 cases, 95% of children under 3 years of age, severe HFMD patients who died of EV71 accounted for 92.2% of the total deaths.

In recent years, the situation of severe HFMD and death caused by CA10 infection has gradually attracted attention. In some areas, CA10 infection can cause severe cases with a frequency of 10.7%, and can even lead to cardiopulmonary failure leading to death.


  1. Exanthema subitum

Exanthema subitum, also known as roseola infantum, sixth disease, is a clinically common acute febrile rash skin disease in infants and young children, mainly caused by (human herpes virus 6, HHV-6 B subtype infection, a small part by HHV -7 caused.

3.1 Typical performance of exanthema subitum

Children with exanthema subitum occur in infants under 2 years of age. It is characterized by sudden high fever. After 3 to 5 days, the body temperature returns to normal. At the same time, the skin has rose-colored papules, which disappear after 1 to 2 days without leaving any traces. The rash usually occurs in the neck and trunk first, and then gradually spreads to the upper and lower limbs. There are no rashes on the face, under the elbows, and in the palms. In addition to loss of appetite, the general mental state of the child has no significant changes, a small number may appear drowsiness, nausea, vomiting and even heat sputum.

3.2 Complications of exanthema subitum

The prognosis of children with acute rash is mostly good, and the complications are rare. The reports of complications are more common in HHV-6 infected patients, including blood system changes, heat sputum, liver dysfunction, respiratory damage, myocardial damage and childhood acute rash-related brain. Inflammation / encephalopathy, etc., can also lead to death.

3.2.1 Blood system changes

The number of neutrophils decreases when the rash occurs. In severe cases, granulocyte deficiency may occur, sometimes accompanied by thrombocytopenia, reticulocyte reduction, and hemoglobin decrease, while lymphocytes are slightly increased, and even atypical lymphocytes are seen, and blood system changes. Often transient, after the condition improves, it can return to normal. The increase of hemophagocytic cells and atypical lymphocytes in the bone marrow suggests that bone marrow cells are affected by HHV-6 infection, and some cytokines such as IFN-γ-induced protein-10, monocyte chemoattractant protein-1 and IFN-γ are also induced. Mononuclear factors may play an important role in neutropenia.

3.2.2 Heat cramp

Children with acute rash and heat sputum are more common. It is reported that the Japanese merger rate is 8%, the combined rate of infants under 1 year old can be as high as 57%, and that in the UK is 13%. At present, the pathogenesis of urticaria in children is still unclear. Kondo and other studies have found that the incidence of HHV-6 DNA in cerebrospinal fluid is high in children with acute rash after 3 years of acute rash. After a hot sputum attack, HHV-6 DNA was almost negative in the cerebrospinal fluid of those who had fever and no sputum. Therefore, HHV-6 is thought to invade the nervous system during primary infection, forming a latent infection, and repeated episodes of thermal paralysis may be related to the reactivation of HHV-6. Kittak et al. performed serum matrix metalloproteinase (MMP-9) and tissue inhibitor of metallopro-teinases-1 (TIMP-1) in children with primary HHV-6 infection. Detection. The results showed that the levels of MMP-9 and TIMP-1 in the serum of the hot sputum group were significantly higher than those in the non-heat sputum group, suggesting that this may lead to dysfunction of the blood-brain barrier and cause thermal paralysis.

3.2.3 Abnormal liver function

Studies have shown that HHV-6 infection can damage liver cells and induce liver function. Children with acute rash can also have abnormal liver function, mainly due to elevated liver enzymes, severe cases can induce liver dysfunction, acute liver failure, and even fulminant hepatitis leading to death. In addition, there are reports of childhood acute rash complicated with tyrosinemia type 1 acute liver failure.

3.2.4 Respiratory damage

In addition to pharyngitis, bronchitis, bronchitis, children with acute rash can also be associated with bronchial pneumonia, suppurative sinusitis, suppurative otitis and other rare symptoms, some can induce acute obstructive bronchitis (bronchitis). In addition, interstitial pneumonia can also be combined.

3.2.5 Myocardial injury

A small number of children with acute rash can be associated with myocardial injury, manifested as sinus arrhythmia, elevated myocardial zymogram or abnormal electrocardiogram, mostly transient, good prognosis. Occasionally, it can cause fatal acute myocarditis.

3.2.6 Exanthem subi-tumassociated encephalitis / encephalopathy

Children with acute rash can cause neurological complications, including febrile seizures and childhood acute rash-related encephalitis/encephalopathy. According to statistics, there are about 60 cases of childhood acute rash-related encephalitis in Japan, which can lead to death and severe neurological sequelae, including limb paralysis and neurodevelopmental delay. Children with acute rash-related encephalitis often occur before rash, including acute necrotizing encephalitis, hemorrhagic shock, encephalopathy syndrome, bipolar sputum and acute diffuse attenuation of acute encephalopathy (AESD), reversible posterior encephalopathy syndrome Wait, even in the early stage, fatal brain damage can occur, and a small number of aseptic meningoencephalitis can occur. The mechanism of HHV-6 causing encephalitis/encephalopathy is still unclear. HHV-6 DNA and various cytokines, including IL-6, soluble TNF receptor 1, IL-1β, IL8, can be detected in the cerebrospinal fluid of children. IL-10, IL12p70, TNF-α, IFN-γ, MMP-9 and MCP-1 suggest that the onset of acute rash in children may be a direct effect of the virus, but it may not be the main effect.


  1. Conclusion

In summary, measles, hand, foot and mouth disease and early childhood acute rash have certain pathogenesis and clinical features, and are also easily misdiagnosed and mistreated due to atypical symptoms. Clinically, they must not only be differentiated from certain skin diseases, but also their systemic manifestations. Or complications should be differentiated from other medical conditions. Like most viral diseases, these three diseases can also heal themselves, with a good prognosis in the absence of serious complications. However, due to the complexity of the development of these diseases in recent years, it is necessary to have sufficient knowledge of them to achieve early diagnosis, early isolation, early treatment, avoid further spread of the disease, relieve the symptoms of patients, prevent the occurrence or aggravation of complications, and avoid the legacy. Aftereffects, etc.

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