bubble_chart Overview

Mucocutaneous lymph node syndrome (MCLS), also known as Kawasaki disease, is an acute febrile eruptive pediatric disease primarily characterized by systemic vasculitis. It was first reported in 1967 by Japanese physician Tomisaku Kawasaki. Due to the potential for severe cardiovascular complications, this condition has drawn significant attention, with an increasing incidence in recent years. In 1990, Beijing Children's Hospital reported 67 cases of Kawasaki disease among hospitalized patients with rheumatic diseases, compared to 27 cases of rheumatic fever. Data from 11 hospitals in other provinces showed Kawasaki disease cases were twice as many as rheumatic fever cases. Clearly, Kawasaki disease has replaced rheumatic fever as one of the leading causes of acquired heart disease in children in China. Currently, Kawasaki disease is considered an immune-mediated vasculitis and is temporarily classified among connective tissue disorders.

bubble_chart Epidemiology

This disease can affect both infants and children, but 80–85% of patients are under 5 years old, with a peak incidence in infants aged 6–18 months. Boys are more commonly affected, with a male-to-female ratio of 1.3–1.5:1. There is no distinct seasonal pattern, though some suggest a higher incidence in summer. By 1990, Japan had reported approximately 100,000 cases of Kawasaki disease, with three epidemics occurring in 1979, 1982, and 1986. During these outbreaks, the incidence rate among children under 4 years old was 172–194 per 100,000. Although fewer cases have been reported worldwide compared to Japan, the disease has been documented in countries ranging from Sweden, the Netherlands, the United States, Canada, the United Kingdom, and South Korea in the north to Greece, Australia, and Singapore in the south. In China, the first few cases were reported in 1978 from Beijing, Shanghai, Hangzhou, Chengdu, and Taiwan. By 1989, the *Journal of Practical Pediatrics* had compiled 220 cases from across the country. A nationwide survey of major children's hospitals and affiliated medical school hospitals from 1983 to 1986 identified 965 hospitalized cases. A second survey from 1987 to 1991 recorded an increase to 1,969 hospitalized cases, with an upward trend annually. Among these, 78.1% were under 4 years old, with a male-to-female ratio of 1.6:1. In the United States, cases are more prevalent among individuals of Japanese descent. Reports from Japan indicate a 1–2% incidence among siblings, suggesting a genetic predisposition.

bubble_chart Etiology

The cause of the disease remains unclear. This disease exhibits certain epidemic and endemic characteristics, with clinical manifestations such as fever and rash, suggesting an association with infection. It is generally believed that multiple pathogens may be involved, including Epstein-Barr virus, retroviruses, or infections by streptococcus and propionibacterium. In 1986, it was reported that the supernatant of peripheral blood lymphocyte cultures from patients showed increased reverse transcriptase activity, indicating that the disease might be caused by a retrovirus. However, most studies have not yielded consistent results. Previously, mycoplasma, rickettsia, and dust mites were proposed as potential pathogens, but these hypotheses have not been confirmed. Some also consider environmental pollution or chemical allergies as possible causative factors.

bubble_chart Pathogenesis

Recent studies have shown that there is significant immune dysregulation during the acute phase of this disease, which plays an important role in the pathogenesis. In the acute phase, there is an imbalance in peripheral blood T-cell subsets, with an increase in CD₄ and a decrease in CD₈, leading to an elevated CD₄/CD₈ ratio. This change is most pronounced at 3–5 weeks of illness and returns to normal by 8 weeks. The increased CD₄/CD₈ ratio puts the body's immune system in an activated state, with CD₄ secreting more lymphokines, promoting polyclonal activation, proliferation, and differentiation of B cells into plasma cells. This results in elevated serum levels of IgM, IgA, IgG, and IgE, as well as activated T cells secreting high concentrations of interleukins (IL-1, 4, 5, 6), gamma-interferon (IFN-γ), and tumor necrosis factor (TNF). These lymphokines and active cytokines can induce endothelial cells to express and produce new antigens; on the other hand, they also promote B cells to secrete autoantibodies, leading to endothelial cell cytotoxicity and endothelial cell injury, thereby causing vasculitis. Elevated IL-1, IL-6, and TNF can also induce hepatocytes to synthesize acute-phase reactive proteins, such as C-reactive protein, α_r-antitrypsin, and haptoglobin, contributing to the acute fever response in this disease. Patients with this disease exhibit elevated circulating immune complexes (CIC), detectable in 50–70% of cases as early as the first week of illness, peaking at weeks 3–4. The mechanism of CIC in this disease remains unclear, but the absence of immune complex deposition in the affected areas and the fact that serum C₃

does not decrease but rather increases do not align with typical immune complex diseases. The trigger for the aforementioned immune dysregulation is unknown. Currently, it is widely believed that Kawasaki disease is an immune-mediated systemic vasculitis triggered by multiple infectious agents in a genetically susceptible host.

bubble_chart Pathological Changes

According to the summary of 217 fatal cases by the Japanese MCLS Research Committee in 1990, the pathological morphology of this disease's vasculitis can be divided into four stages:

**Stage I**: Approximately 1–2 weeks, characterized by: ① Inflammation of small arteries, small veins, microvessels, and their surrounding tissues; ② Inflammation of medium and large arteries and their surrounding tissues; ③ Infiltration of lymphocytes and other white blood cells, along with local edema.

**Stage II**: Approximately 2–4 weeks, characterized by: ① Reduced inflammation in small vessels; ② Predominant inflammation in medium arteries, often with coronary artery aneurysms and thrombosis; ③ Rare vascular inflammation in large arteries; ④ Prominent mononuclear cell infiltration or necrotic changes.

**Stage III**: Approximately 4–7 weeks, characterized by: ① Subsiding inflammation in small vessels and microvessels; ② Granuloma formation in medium arteries.

**Stage IV**: Approximately 7 weeks or longer, where acute vascular inflammation mostly disappears, replaced by thrombosis, obstruction, intimal thickening leading to aneurysms, and scar formation in medium arteries. Regarding the distribution of arterial lesions, they can be categorized as: ① Extrinsic medium or large arteries, often involving coronary, axillary, iliac arteries, and other arteries in the neck, chest, and abdomen; ② Intrinsic arteries within organs, affecting the heart, kidneys, lungs, gastrointestinal tract, skin, liver, spleen, gonads, salivary glands, brain, and other systemic organs.

Beyond vasculitis, the pathology also involves multiple organs, particularly interstitial myocarditis, pericarditis, and endocarditis, which are most prominent and may affect the conduction system, often leading to death during Stage I. By Stages II and IV, ischemic heart disease is common, and myocardial infarction may cause death. Additionally, aneurysm rupture and myocarditis are significant causes of death in Stages II and III.

The vascular pathology of MCLS is very similar to infantile polyarteritis nodosa. Apart from coronary or pulmonary artery aneurysms and thrombosis, changes are also observed in the intima of major arteries, ileal arteries, or pulmonary arteries. Fluorescent antibody tests reveal immunoglobulin IgG deposits in the arterial walls of the heart, spleen, and lymph nodes. Vascularitis may occur in cervical lymph nodes and skin, accompanied by small vessel fibrinoid necrosis. Other findings include severe thymic atrophy, increased heart weight, hypertrophic ventricular dilation, grade I hepatic fatty degeneration, and lymph node congestion with follicular enlargement. However, the glomeruli show no significant lesions.

The differences between this disease and classic polyarteritis nodosa (Kussmaul-Maier type) are as follows: ① The latter exhibits marked fibrinoid necrosis in vasculitis, whereas MCLS rarely shows such necrotic changes or only mild ones; ② Classic polyarteritis nodosa rarely involves the pulmonary arteries.

bubble_chart Clinical Manifestations

Main symptoms: Common persistent fever lasting 5–11 days or longer (2 weeks to 1 month), with body temperature often reaching above 39°C, unresponsive to antibiotic treatment. Bilateral conjunctival congestion, flushed lips with rhagades or bleeding, and a "Chinese wax myrtle bark"-like tongue are frequently observed. Hard edema appears in the hands, with early erythema on the palms and soles, followed by characteristic large-scale peeling of the fingertips after 10 days, occurring at the junction of the nail bed and skin. Acute non-suppurative transient cervical lymphadenopathy is also present, most prominent in the anterior neck, with a diameter of about 1.5 cm or more, mostly unilateral, slightly tender, occurring within 3 days of fever, and resolving spontaneously after a few days. Shortly after fever onset (approximately 1–4 days), maculopapular or polymorphous erythema-like rashes appear, occasionally miliaria-like rashes, mostly on the trunk, without vesicles or crusting, and fading in about a week.

Other symptoms: Cardiac involvement often occurs, manifesting as myocarditis, pericarditis, and endocarditis. Patients exhibit an accelerated pulse, and auscultation may reveal tachycardia, gallop rhythm, and muffled heart sounds. Systolic murmurs are also common. Valvular insufficiency and heart failure may develop. Echocardiography and coronary angiography can detect coronary artery aneurysms, pericardial effusion, left ventricular enlargement, and mitral regurgitation in most patients. Chest X-rays may show cardiomegaly. Occasionally, joint pain or swelling, cough, rhinorrhea, abdominal pain, grade I jaundice, or aseptic meningoencephalitis may occur. In the acute phase, about 20% of cases exhibit perineal and perianal skin erythema and desquamation, with reappearance of erythema or crusting at the site of BCG vaccination 1–3 years prior. During the convalescent stage, transverse grooves may appear on the nails.

The course varies in length. The initial stage (first stage) is the acute febrile phase, typically lasting 1–11 days, during which major symptoms appear progressively after fever onset, and severe myocarditis may occur. The intermediate stage (second stage) is the subacute phase, usually spanning days 11–21, marked by resolution of fever in most cases and symptom relief, with membranous desquamation of the fingertips. Severe cases may still experience persistent fever. Coronary artery aneurysms may develop, leading to myocardial infarction or aneurysm rupture. Most patients enter the late stage (third stage), or convalescent phase, by the 4th week (days 21–60), during which clinical symptoms subside, and recovery progresses if no significant coronary artery lesions are present. However, coronary artery aneurysms may persist or progress, potentially causing myocardial infarction or ischemic heart disease. A few severe cases with coronary artery aneurysms enter a chronic phase, lasting years, with residual coronary artery stenosis, leading to angina, cardiac dysfunction, or ischemic heart disease, which may be life-threatening due to myocardial infarction.

bubble_chart Auxiliary Examination

During the acute phase, the total white blood cell count and the percentage of granulocytes increase, with a left shift in nuclear morphology. More than half of the patients exhibit grade I anemia. The erythrocyte sedimentation rate (ESR) is significantly elevated, reaching over 100mm in the first hour. Serum protein electrophoresis shows an increase in globulins, particularly a significant rise in α₂ globulin. Albumin levels decrease, while IgG, IgA, and IgA levels are elevated. Platelet counts begin to rise in the second week, and the blood exhibits a hypercoagulable state. The anti-streptolysin O (ASO) titer is normal. Rheumatoid factor and antinuclear antibodies are negative. C-reactive protein levels are elevated. Blood moistening and tonifying levels are normal or slightly elevated. Urinary sediment may show increased white blood cells and/or proteinuria. Electrocardiograms (ECGs) reveal various abnormalities, most commonly ST-segment and T-wave changes, as well as prolonged P-R and Q-R intervals, abnormal Q waves, and arrhythmias. Two-dimensional echocardiography is suitable for cardiac examination and long-term follow-up, detecting various heart blood vessel abnormalities in half of the cases, such as pericardial effusion, left ventricular enlargement, mitral regurgitation, and coronary stirred pulse dilation or the formation of stirred pulse aneurysms. It is recommended to perform this examination weekly during the acute and subacute phases of the disease, as it is the most reliable non-invasive method for monitoring coronary stirred pulse aneurysms. In cases of aseptic brain membrane inflammation, cerebrospinal fluid lymphocyte counts may reach 50–70/mm³. Some cases may show slightly elevated serum bilirubin or alanine aminotransferase levels. Bacterial cultures and viral isolation yield negative results.

bubble_chart Diagnosis

The Japanese MCLS Research Committee (1984) proposed that the diagnostic criteria for this disease should meet at least five of the following six main clinical symptoms to be confirmed: ① Fever of unknown origin, lasting 5 days or longer; ② Bilateral conjunctival congestion; ③ Diffuse congestion of the oral and pharyngeal mucosa, red and cracked lips, and a strawberry tongue; ④ Hard swelling of the hands and feet and redness of the palms and soles in the initial stage [first stage] of the illness, followed by membranous desquamation of the fingertips and toes during the recovery phase; ⑤ Polymorphous erythema on the trunk, without vesicles or crusting; ⑥ Non-suppurative swelling of cervical lymph nodes, with a diameter of 1.5 cm or larger. However, if coronary artery aneurysms or dilation are detected by two-dimensional echocardiography or coronary angiography, a diagnosis can be confirmed with four positive main symptoms.

In recent years, reports of incomplete or atypical cases have increased, accounting for approximately 10–20%. These cases exhibit only 2–3 main symptoms but have typical coronary artery lesions. They mostly occur in infants. The incidence of coronary artery aneurysms is similar between typical and atypical cases. Once Kawasaki disease is suspected, echocardiography should be performed as early as possible.

bubble_chart Treatment Measures

Acute phase treatment

1. Gamma globulin: Recent studies have confirmed that early intravenous administration of gamma globulin combined with oral aspirin can reduce the incidence of coronary artery aneurysms in Kawasaki disease. It must be emphasized that the medication should be administered within 10 days of onset. The dosage is 400 mg/kg of gamma globulin intravenously per day, infused over 2–4 hours, for 4 consecutive days; simultaneously, oral aspirin is given at 50–100 mg/kg per day, divided into 3–4 doses, for 4 consecutive days, then reduced to 5 mg/kg per day, administered at draught.
2. Aspirin: Early oral aspirin can control the acute inflammatory process and mitigate coronary artery lesions, but no controlled studies have shown that aspirin treatment reduces the incidence of coronary artery aneurysms. The dose is 30–100 mg/kg per day, divided into 3–4 doses. Japanese doctors tend to use smaller doses, based on the observation that acute-phase Kawasaki disease patients exhibit reduced absorption and increased clearance of aspirin, requiring higher doses to achieve anti-inflammatory effects. After 14 days, once fever subsides, the dose is reduced to 3–5 mg/kg per day, administered at draught, to exert an antiplatelet aggregation effect.
3. Corticosteroids: Adrenal corticosteroids have long been considered to have strong anti-inflammatory effects and can alleviate symptoms. However, it was later discovered that corticosteroids can easily lead to thrombosis, hinder the repair of coronary artery lesions, and promote aneurysm formation. Therefore, corticosteroids such as prednisone should not be used alone. Unless severe myocarditis or persistent high fever occurs in severe cases, prednisone and aspirin may be combined. Generally, corticosteroids are not used alone to control the early inflammatory response in Kawasaki disease.

Treatment during the convalescent stage

1. Anticoagulation therapy: During the convalescent stage, aspirin is administered at 3–5 mg/kg per day, taken once daily, until the erythrocyte sedimentation rate and platelet count return to normal. If no coronary artery abnormalities are present, the medication is usually discontinued 6–8 weeks after onset. Follow-up echocardiography is performed at 6 months and 1 year. For patients with chronic coronary artery lesions, long-term anticoagulation therapy and close follow-up are required. Patients with small, solitary coronary artery aneurysms should take aspirin long-term at 3–5 mg/kg per day until the aneurysm resolves. For those intolerant to aspirin, dipyridamole may be used at 3–6 mg/kg per day, divided into 2–3 doses. Annual cardiac evaluations are necessary. If echocardiography, clinical data, or exercise tests suggest myocardial ischemia, coronary angiography should be performed. Patients with multiple or large coronary aneurysms should take aspirin and dipyridamole long-term. Patients with giant aneurysms are prone to thrombosis, coronary artery stenosis, or occlusion and may require oral warfarin anticoagulation. These patients should limit physical activity and avoid sports. Cardiac evaluations should be performed every 3–6 months. If myocardial ischemia is evident or exercise tests are positive, coronary angiography should be performed to assess the progression of stenosis. Patients with occlusion of one or more major coronary arteries should receive long-term anticoagulation therapy, undergo repeated cardiac evaluations (including myocardial scans, exercise tests, and coronary angiography), and consider surgical treatment.
2. Thrombolytic therapy: For patients with myocardial infarction and thrombosis, intravenous or catheter-based percutaneous coronary artery administration is used to promote coronary recanalization and myocardial reperfusion. Intravenous thrombolysis involves administering 20,000 U/kg of urokinase within 1 hour, followed by 3,000–4,000 U/kg per hour. For coronary artery administration, 1,000 U/kg of urokinase is given within 1 hour. Streptokinase may also be used, with 10,000 U/kg administered intravenously within 1 hour, and another dose given after 30 minutes if needed. These drugs rapidly dissolve fibrin, are highly effective, and have no adverse effects.
3. Coronary angioplasty: In recent years, balloon catheters have been successfully used to dilate stenotic coronary arteries.
4. Surgical treatment: The indications for coronary artery bypass grafting are: ① high-grade occlusion of the left main trunk; ② high-grade occlusion of multiple branches; ③ high-grade occlusion of the proximal left anterior descending artery. For cases of severe mitral regurgitation that are unresponsive to medical therapy, valvuloplasty or valve replacement may be performed. A Japanese study reported 62 Kawasaki disease patients who underwent coronary artery bypass grafting, 7 of whom also underwent mitral valve surgery. Preoperatively, 70% of the patients had angina pectoris, heart failure, or other symptoms. The 4-year survival rate postoperatively was 87%, and the 10-year survival rate was 45%, with most deaths attributed to late-stage [third stage] myocardial infarction or sudden death.

In cases of cardiogenic shock, heart failure, or arrhythmia, appropriate treatment should be administered.

bubble_chart Prognosis

The vast majority of children have a good prognosis, with a self-limiting course, and gradual recovery can be achieved with appropriate treatment. This differs significantly from infantile polyarteritis nodosa.

15–30% of Kawasaki disease patients may develop coronary artery aneurysms. Death due to coronary artery aneurysms, thrombotic occlusion, or myocarditis accounts for 1–2% of all cases, and sudden death may even occur during the convalescent stage. The incidence of residual ischemic heart disease is very low. Recurrence occurs in about 2% of cases. The mortality rate has recently declined to 0.5%–1.0%. An analysis of 104 Kawasaki disease-related deaths in Japan showed myocardial infarction in 57%, heart failure in 12%, myocardial infarction accompanied by heart failure in 6.7%, coronary artery aneurysm rupture in 5%, arrhythmia in 1%, and other causes such as concurrent infections.

Since 1986, Beijing Children's Hospital has examined 188 Kawasaki disease cases using two-dimensional echocardiography, detecting coronary artery lesions in 60 cases, including dilation in 44 and aneurysm formation in 16. Follow-up ranged from 3 months to 5 years, with an average of 22.6 months. Among them, 40 cases of dilation and 6 cases of aneurysms returned to normal. The recovery times were 4.4 ± 2.9 months and 15.7 ± 17.2 months, respectively. Two deaths occurred: one with multiple grade II coronary artery aneurysms (internal diameter 7mm) due to acute anterior wall myocardial infarction, and another with multiple giant aneurysms, which resulted in right coronary artery rupture on day 28 of the disease course.

bubble_chart Complications

Due to the pathological changes in the coronary arteries, which are both symptoms of the disease itself and potentially fatal complications, this section will detail their progression to facilitate early detection and timely appropriate treatment.

1. Coronary artery lesions: According to observations of 1,009 cases of Kawasaki disease in Japan, transient coronary artery dilation accounted for 46%, while coronary artery aneurysms accounted for 21%. Two-dimensional echocardiography revealed that coronary artery dilation could appear as early as the third day of illness, with most cases resolving within 3 to 6 months. Coronary artery aneurysms could be detected by the sixth day of illness, with the highest detection rate occurring in the second to third weeks. New lesions rarely appeared after the fourth week. The incidence of coronary artery aneurysms was 15–30%, and the presence of clinical myocarditis did not predict coronary artery involvement. Some well-established risk factors associated with coronary artery aneurysms included age of onset under 1 year, male gender, persistent fever exceeding 14 days, anemia, total white blood cell count above 30×10⁹/L, erythrocyte sedimentation rate over 100 mm/h, significantly elevated C-reactive protein, reduced plasma albumin, and the presence of peripheral artery aneurysms. Most coronary artery aneurysms followed a self-limiting course, with the majority resolving spontaneously within 1 to 2 years. The coronary artery lesions in this disease most commonly affected the proximal main trunk and the left anterior descending branch, followed by the left circumflex branch, which was less common. Isolated distal artery aneurysms were rare. The severity of coronary artery lesions is generally classified into four grades: ① Normal (Grade 0): No coronary artery dilation. ② Grade I: Significant but localized aneurysmal dilation, with an internal diameter <4 mm. ③ Grade II: May be single, multiple, or extensive, with an internal diameter of 4–7 mm. ④ Grade III: Giant aneurysms with an internal diameter ≥8 mm, often extensive and involving more than one branch. The incidence is approximately 5%, with a poor prognosis. Therefore, patients with coronary artery lesions should undergo close follow-up and regular echocardiographic examinations. Typically, examinations should be performed weekly within the first 4 weeks of illness, then at 2 months, 6 months, and at least annually thereafter, depending on the severity of the lesions. Symptomatic patients and those with severe coronary artery involvement should undergo coronary angiography. Angiography can accurately assess the degree of coronary artery stenosis, occlusion, and distal lesions. Due to transient myocardial ischemia or ventricular fibrillation caused by distal occlusion, severe complications may occur. Indications for coronary angiography include: ① Symptoms of myocardial ischemia. ② Persistent cardiac valvular lesions. ③ X-ray plain films showing coronary artery calcification. ④ Echocardiography revealing persistent coronary artery aneurysms.
2. Gallbladder hydrops: Often occurs during the subacute phase and may present with severe abdominal pain, abdominal distension and fullness, and jaundice. A mass may be palpable in the right upper quadrant, which can be confirmed by abdominal ultrasound. Most cases resolve spontaneously, though occasional complications such as paralytic ileus or intestinal hemorrhage may occur.
3. Arthritis or arthralgia occurs during the acute or subacute phase, affecting both large and small joints in approximately 20% of cases, resolving as the condition improves.
4. Neurological changes: During the acute phase, these include aseptic meningoencephalitis, facial nerve palsy, hearing loss, acute encephalopathy, and febrile seizures, all caused by vasculitis. These are clinically common, recover quickly, and have a good prognosis. Among these, aseptic meningoencephalitis is the most common, with an incidence of about 25%, mostly occurring within the first 2 weeks of illness. Some children exhibit increased intracranial pressure, presenting with bulging fontanelles. A few children may have neck stiffness, drowsiness, fixed gaze, unconsciousness, or other disturbances of consciousness. Cerebrospinal fluid shows grade I lymphocytosis, with normal glucose and chloride levels, and protein levels are mostly normal. Clinical symptoms usually resolve within a few days. Facial nerve palsy is more common in severe cases, often presenting as peripheral palsy, possibly due to vasculitic reactions affecting the facial nerve or adjacent vascular lesions such as aneurysm formation or artery dilation, leading to transient compression of the facial nerve. During the convalescent stage, limb paralysis caused by middle cerebral artery stenosis or occlusion may leave sequelae, though this is relatively rare.
5. Other complications: Pulmonary vasculitis may present as increased lung markings or patchy shadows on chest X-rays, with occasional pulmonary infarction. During the acute phase, urethritis may occur, and urine sediment may show increased white blood cells and grade I proteinuria. Iridocyclitis is relatively rare. Approximately 2% of patients develop arterial aneurysms, most commonly in the axillary and iliac arteries. Digital gangrene is occasionally observed.

bubble_chart Differentiation

It should be differentiated from various eruptive pestilential diseases, viral infections, acute lymphadenitis, Bi disease, and other connective tissue diseases, viral myocarditis, and wind-dampness carditis.

The differences between this condition and scarlet fever are: ① the rash begins on the third day after onset; ② the rash morphology resembles measles and erythema multiforme; ③ the susceptible age is infancy and early childhood; ④ penicillin is ineffective.

The differences between this condition and juvenile Bi disease are: ① the fever period is shorter, and the rash is more transient; ② hard swelling of hands and feet, often showing metatarsal flushing; ③ negative rheumatoid factor.

The differences from exudative erythema multiforme are: ① no purulent discharge or pseudomembrane formation in the eyes and lips; ② the rash does not include blisters or crusts.

The differences from systemic lupus erythematosus are: ① the rash is not prominent on the face; ② total white blood cell count and platelets are generally elevated; ③ antinuclear antibodies are negative; ④ the susceptible age is infancy, and it is more common in boys.

There are many similarities with infantile nodular stirred pulse syndrome, but MCLS has a higher incidence, shorter course, and better prognosis. The relationship between these two diseases remains to be studied.

The differences from eruptive sexually transmitted viral infections are: ① red, dry, cracked, and bleeding lips, resembling Chinese wax myrtle bark tongue; ② hard swelling of hands and feet, often with metatarsal flushing and late-stage [third stage] membranous desquamation of fingertips and toes; ③ no edema or discharge in the conjunctiva; ④ elevated total white blood cell count and granulocyte percentage, with a left shift; ⑥ significantly increased ESR and C-reactive protein.

The differences from acute lymphadenitis are: ① cervical lymphadenopathy and tenderness are milder, with no local skin or subcutaneous tissue redness; ② no purulent lesions.

The differences from viral myocarditis are: ① prominent coronary stirred pulse lesions; ② characteristic changes in hands and feet; ③ persistent high fever.

The differences from wind-dampness carditis are: ① prominent coronary stirred pulse lesions; ② no significant heart murmurs; ③ the primary affected age group is infants and young children.