Measles (measles, rubeola, morbilli) is an acute respiratory pestilence caused by the measles virus. The main symptoms include fever, upper respiratory tract inflammation, conjunctivitis, etc., characterized by the appearance of red papules on the skin and measles mucous membrane spots on the buccal mucosa. This Bingchuan is highly contagious and prone to epidemics in densely populated areas without widespread vaccination. Major outbreaks occur approximately every 2 to 3 years. Since 1965, when China began widespread vaccination with the measles attenuated live vaccine, major outbreaks have been controlled.

bubble_chart Epidemiology

1. Measles is highly contagious, with humans being the only natural host. Acute patients are the most significant source of infection. It is generally believed that asymptomatic carriers and measles virus carriers are few in number and have very low infectivity.
2. Transmission routes and methods: The disease is primarily spread through the respiratory tract. From the late incubation period to the early stage of full eruption, the patient's oral, nasal, pharyngeal, and ocular mucosal secretions contain a large amount of the virus. When the patient speaks, coughs, or sneezes, the virus can be dispersed into the surrounding air via droplets, entering susceptible individuals through the nasopharynx or conjunctiva. Close contacts can also spread the virus through contaminated hands. The infectious period of the disease generally lasts from five days before the eruption to five days after the eruption. Infectivity begins as early as the seventh day of the incubation period, but it is strongest from the late incubation period to the first or second day after the eruption. If the patient develops pneumonia, the infectious period may extend to ten days after the eruption. Indirect transmission through clothing or utensils is rare.
3. Susceptible individuals: Anyone who has not had measles or received the measles vaccine is susceptible. Most newborns acquire passive immunity from their mothers via the placenta. This immunity lasts for 4–6 months, gradually declining thereafter. By nine months, antibody levels are undetectable, but it is believed that this immunity can still interfere with the effectiveness of the live measles vaccine until 15 months of age. Before widespread vaccination, the peak incidence of measles in China occurred between 6 months and 5 years of age. However, since the widespread use of the vaccine, the age of onset has shifted upward. According to data from Shanghai, the 6-month to 5-year and 5–9-year age groups each account for 40% of cases. In northern China, a 1985 report indicated that 67% of cases occurred in individuals aged 14–23. In the United States, 25% of cases in 1977 were among adolescents. If the mother has not had measles, the newborn can also contract the disease.
4. Epidemiological situation: Measles typically exhibits regional outbreaks. In areas without widespread vaccination, when the susceptible population accumulates to over 40%, large outbreaks can occur in densely populated cities, approximately every 2–3 years. In rural, remote, or mountainous areas with dispersed populations and limited transportation, the intervals between outbreaks are longer. Measles is highly contagious, with nearly 90% of susceptible individuals living with the patient (in the same household or childcare facility) becoming infected. The disease is more common in winter and spring but can occur year-round. There is no gender difference. After infection, lasting immunity is acquired, and second infections are rare.

1. A significant decline in incidence and the flattening of epidemic peaks: Before liberation, the incidence rate in China was approximately 5,000 per 100,000. By 1958, it had dropped to 1,000 per 100,000. After nationwide vaccination began in 1965, the incidence rate declined year by year, falling to 8.9 per 100,000 by 1988. In the United States, after vaccination began in 1963, the incidence rate dropped to 0.7 per 100,000 by 1982. As the incidence rate declined, epidemic peaks also flattened significantly, with cases mostly sporadic or localized.
2. Extended and less distinct intervals between outbreaks: Before widespread vaccination, the interval between outbreaks was related to population density. When the susceptible population accumulated to a certain percentage, an outbreak would occur—every 1–3 years in cities and every 2–6 years in rural areas. After widespread vaccination, this pattern became less distinct, and the intervals between outbreaks lengthened.
3. A shift in the age of onset: Before widespread vaccination, 98% of cases occurred in children under 10 years old, with 80% in the 0–4 age group. After vaccination, a 1992–1993 outbreak in Guangxi showed that only 18.0% of cases were in the 0–4 age group, while over 80% were in children over 5 and adolescents. Similar trends were observed abroad. Before vaccination, most cases were in children under 10. In the United States, after vaccination, 57% of cases in 1987 were among adolescents aged 9–19.
4. The clinical manifestations of prevalent cases are increasingly mild and atypical. After widespread vaccination, the majority of patients during outbreaks exhibit mild symptoms, with severe cases significantly reduced and complications becoming rare. The mortality rate has markedly declined. After an outbreak, 5–15% of the population without a history of measles show elevated antibody levels. It is believed that with a hemagglutination inhibition antibody titer ≥1:16 post-vaccination, measles infection is unlikely. As antibody levels decline, the rate of subclinical infections rises. A 1987 report from a county in Zhejiang showed subclinical infection rates of 14.3% for those with antibody titers of 1:8, 32.7% for 1:4, and rising to 83.3% for 1:2.

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bubble_chart Pathogen

The measles virus (Morbillivirus) belongs to the Paramyxoviridae family and differs from other paramyxoviruses by lacking neuraminidase. Under electron microscopy, it appears spherical or polymorphic, with a larger diameter of 100–250 nm. The viral core consists of ribonucleic acid (RNA) and a symmetrically helical capsid, enveloped by a double-layered lipoprotein membrane with small surface spikes containing hemagglutinin. The measles virus primarily comprises six structural proteins: three associated with RNA—the F protein, which functions as a polymerase; the N protein, which stabilizes the genome; and the P protein, which acts as a polymerase. The other three structural proteins are associated with the outer membrane: the M protein, a membrane protein involved in viral assembly, budding, and replication; the H protein, a surface hemagglutinin that binds to receptors during viral attachment to susceptible host cells; and the F protein, which has fusion properties, enabling the viral membrane to merge with the host cell membrane for viral entry. The virus can be cultured in human embryonic and monkey kidney cells, inducing multinucleated giant cells and intranuclear inclusion bodies within 5–10 days. There is only one serotype of the measles virus. During the eruption phase in patients, specific antibodies can be detected in the blood. The virus is inactivated by heat, ultraviolet light, lipid solvents like ether and chloroform, as well as extreme pH levels (<5 or >10). Proteins protect the virus from heat and light damage. At room temperature, the virus typically survives for only 36 hours and is inactivated by heating at 56°C for 15–30 minutes. It is resistant to drying and cold, remaining viable for over five years at -70°C and up to 20 years when freeze-dried. Due to its weak survival outside the host, the virus loses its infectivity within half an hour after a patient leaves the room if windows are opened for ventilation.

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After the measles virus invades the human body through droplet particles, its infection process, based on animal experiments, is shown in Table 11-11.

Table 11-11 Measles Infection Process

The measles virus invades the primary site, replicates there, and rapidly spreads to local lymphoid tissues. It is carried by macrophages or lymphocytes through the bloodstream (primary viremia) to reach systemic reticuloendothelial cells, where it extensively replicates, causing a secondary large-scale viremia that disseminates to tissues and organs throughout the body, leading to measles lesions. During the infection process, in addition to the direct invasion of host cells by the virus causing lesions, the body also undergoes a series of immune responses. The virus stimulates T lymphocytes, causing them to differentiate and proliferate extensively, becoming sensitized lymphocytes. When these lymphocytes come into contact with viral antigens, they release lymphokines, leading to mononuclear cell infiltration, inflammatory responses, and even tissue necrosis at the lesion sites. These virus-sensitized lymphocytes primarily exhibit blastogenic and cytotoxic effects, causing infected cells to enlarge, fuse, and form multinucleated giant cells, as well as inducing cytotoxic changes. Therefore, some believe that the measles process is a systemic delayed-type hypersensitivity cell-mediated immune response.

Immune response: After contracting measles, normal individuals exhibit an immune response. By the 14th day of the disease course, hemagglutination inhibition, complement fixation, and neutralizing antibodies can be detected. Antibody titers gradually increase, peaking at 4–6 weeks. Complement-fixing antibodies disappear relatively quickly, while hemagglutination inhibition and neutralizing antibodies decline to one-fourth within a year. Some reports indicate that if there is no re-exposure to measles after natural infection, antibody titers may drop to 1/16 over 15 years, though most individuals maintain low levels for life. IgM appears early and persists for up to 6 weeks, while secretory IgA (SIgA) can be detected in respiratory secretions. Blood IgG persists for a longer duration. The body typically produces corresponding antibodies against different viral structural proteins: H protein antibodies prevent viral adsorption and can also be detected during eruption, showing a significant rise over 2–3 cycles of day and night; F antibodies inhibit viral spread within cells but remain at relatively low levels; NP antibodies test positive during eruption, rise rapidly, and maintain high titers; M antibodies are positive in only half of cases early on and exhibit low titers.

The cellular immune response plays an important role in the pathogenesis of measles. The recovery process from measles infection is associated with an increase in blood and secretory antibodies, the appearance of interferon (around days 6–11), and the enhancement of cellular immunity, with the latter being the most crucial. Individuals with cellular immune deficiencies or impairments (such as leukemia, cancer patients, those on immunosuppressive drugs, or those with congenital immune deficiencies) cannot eliminate the virus and are thus prone to severe, prolonged measles, which can be fatal. Even the administration of large doses of passive immune antibodies is ineffective. On the other hand, individuals with agammaglobulinemia can recover smoothly if they contract measles, indicating that antibodies are not essential for recovery from measles. However, specific antibodies do have a definitive effect in preventing measles infection.

During the course of measles, nonspecific immunity declines, such as a reduction in total white blood cell and neutrophil counts, as well as impaired neutrophil motility. T and B lymphocytes, complement components C_1q, C₄, C₃, C₅, and platelets all show varying degrees of decrease. For example, the tuberculin skin test may turn negative within 2–6 weeks of the rash onset, often exacerbating pre-existing tuberculous lesions. The reduction in immune responses may temporarily alleviate symptoms in patients with eczema, asthma, or nephrotic syndrome.

bubble_chart Pathological Changes

The characteristic pathological changes of measles involve extensive cell fusion forming multinucleated giant cells, known as Warthin-Finkeldey giant cells. These cells vary in size (15–100 μm) and contain dozens to hundreds of nuclei, with eosinophilic inclusion bodies present both inside and outside the nuclei, particularly abundant in the cytoplasm. Under electron microscopy, the inclusion bodies display neatly arranged viral nucleocapsids. These giant cells are widely distributed in the reticuloendothelial system, such as lymph nodes, tonsils, and thymus. Another type, called epithelial giant cells, is primarily found in the respiratory epithelium and also exhibits intranuclear and extranuclear eosinophilic inclusion bodies. These giant cells often detach from the epithelial surface and can be identified in secretions.

In addition to systemic lymphoid tissue hyperplasia, respiratory lesions are prominent, with swelling, congestion, and lymphocyte infiltration observed from the nasopharynx to the trachea, bronchi, and bronchioles. Epithelial multinucleated giant cells can be identified, and the lumens are filled with inflammatory exudate. The lungs exhibit interstitial pneumonia, with alveolar wall cell proliferation, infiltration, and edema, along with the appearance of multinucleated giant cells. In severe cases, measles giant cell pneumonia may develop. Secondary bacterial infections can lead to extensive bronchopneumonia. Skin rash biopsies reveal proliferation of capillary endothelial cells in the dermis, edema, mononuclear cell infiltration, and plasma and red blood cell extravasation, leading to pigmented spots. Subsequently, epidermal cell degeneration occurs, accompanied by multinucleated giant cells, intercellular edema, vacuolation, necrosis, and eventual keratinization and desquamation. The lesions of oral measles mucosal spots (Koplik's spots) are similar to those of the rash, with mucosal and submucosal edema, but the number of multinucleated giant cells is greater, containing more nuclei, and edema is more pronounced than inflammation. In cases complicated by encephalitis, brain tissue may exhibit congestion, edema, perivascular inflammatory infiltration, and even demyelination. Severe cases may also involve cloudy swelling and fatty degeneration in the liver, heart, and kidneys.

bubble_chart Clinical Manifestations

The incubation period is relatively regular, approximately 10±2 days, but can extend to 20–28 days in individuals with passive immunity. Low-grade fever may occur at the end of the incubation period. Typical childhood measles can be divided into the following late stage [third stage].

1. Prodromal stage: From onset to eruption, it lasts about 3–5 days. The main symptoms include fever and upper respiratory catarrhal symptoms. The fever is generally mild to moderate, though sudden high fever with convulsions may occur. Symptoms such as runny nose, irritating dry cough, conjunctival congestion, tearing, and photophobia gradually worsen, accompanied by lethargy, anorexia, and dry rales audible in the lungs. Young children often experience vomiting and diarrhea. Transient small red enanthem may appear on the soft and hard palate. On days 2–3 of illness, small grayish-white sand-like spots surrounded by redness may appear on the buccal mucosa near the molars on both sides, known as measles mucosal spots (Koplik's spots), which are an early characteristic of the disease. These spots may gradually increase and merge, and can also appear on the inner side of the lower lip and gingival mucosa, occasionally on the hard palate. They typically last 16–18 hours, sometimes extending to 1–2 days, and mostly disappear within 1–2 days after the eruption.
2. Stage of full eruption: About 3–5 days after onset, systemic and upper respiratory symptoms worsen, with body temperature possibly rising to 40°C, accompanied by lethargy, drowsiness, and anorexia. The rash first appears behind the ears and along the hairline, rapidly spreading to the face and neck, then descending to the chest, back, abdomen, and limbs within a day, reaching the palms and soles in about 2–3 days. By this time, the rash on the head and face may begin to fade. The rash is approximately 2–3 mm in size, initially light red and scattered, later becoming denser and bright red, then turning dark red, with normal skin between the rashes. During eruption, systemic lymph nodes, liver, and spleen may enlarge, and coarse dry rales may be heard in the lungs.
3. Stage of convalescence: After the rash fully erupts, it fades in the order of eruption, leaving brown pigmentation with bran-like desquamation, which persists for about 2–3 weeks. As the rash fades, systemic toxic symptoms lessen, fever subsides, and mental state and appetite improve, with cough resolving and recovery occurring. The entire course lasts about 10–14 days.

1. Mild type: Mostly seen in individuals with some immunity, such as infants under 5–6 months, those recently receiving immunoglobulins, blood transfusions, or vaccinations. Systemic and respiratory symptoms are mild. The rash is scattered, leaves no pigmentation, and may even be absent, with no oral mucosal spots. The course is short.
2. Non-eruptive type: In immunocompromised patients, such as those with leukemia, malignant tumors, or congenital immunodeficiency, or those on immunosuppressants, measles may present without rash or mucosal spots, requiring epidemiological and laboratory diagnosis. Some believe that certain diseases in adulthood, such as immune-reactive diseases, seborrheic skin diseases, degenerative bone and cartilage diseases, and tumors, may be linked to non-eruptive measles virus infection in childhood.
3. Severe type: Mostly seen in immunocompromised individuals, such as those with malnutrition or other diseases, or complications like pneumonia or cardiovascular insufficiency. High fever and severe toxic symptoms are common, often accompanied by circulatory heart failure and central nervous system symptoms like dyspnea, tachycardia, cyanosis, drowsiness, unconsciousness, and convulsions. The rash may be densely confluent, faint and barely visible, or appear and fade repeatedly. Hemorrhagic rashes or even large ecchymoses may occur, accompanied by internal bleeding, known as hemorrhagic measles, which has a poor prognosis.
4. Neonatal measles: If the mother contracts measles a few days before delivery, the newborn may develop measles, presenting with catarrhal symptoms, fever, and dense rash.
5. Adult measles: Adults without immunity to measles virus who contract the disease generally exhibit more severe clinical symptoms but fewer complications. Pregnant women with measles may experience late abortion, premature labor, or stillbirth, and newborns may develop measles. During an adult measles outbreak abroad in 1982, confirmed by hemagglutination inhibition tests, the clinical features included:
   1. Prominent gastrointestinal symptoms, with diarrhea, vomiting, and abdominal pain being common;
   2. Frequent accompanying symptoms such as myalgia, back pain, and arthralgia;
   3. 86% of patients experienced liver function impairment;
   4. Koplik's spots persist for a long time, approximately 3 to 5 days;
   5. only complain of eye pain with little photophobia.
6. Atypical measles, also known as atypical measles syndrome, mostly occurs 6 months to 6 years after vaccination with inactivated measles vaccine, upon re-exposure to natural measles patients, or during administration of inactivated measles vaccine. It is occasionally seen in individuals who have previously received live attenuated vaccine. The onset is acute with high fever, accompanied by headache, myalgia, vomiting, dry cough, severe toxic symptoms but few catarrhal symptoms, and rare mucous membrane spots. Two to three days after onset, the rash first appears on the limbs and spreads centripetally, mostly limited to the lower body, initially presenting as yellow-red maculopapules, followed by petechiae, vesicles, urticaria, etc., exhibiting polymorphism. The rash resolves without leaving spots or scabs, often complicated by pneumonia, pleural effusion, and pulmonary shadows that may persist for several months to 1–2 years. During the convalescence stage, by the 10th day of the disease course, extremely high measles complement-fixing antibodies and hemagglutination-inhibiting antibodies can be detected, with titers reaching >1:1280. To date, measles virus has not been isolated from such patients, and it appears non-epidemic. Most believe its pathogenesis is due to the inactivated vaccine only inducing HI antibodies without eliciting antibodies against the F protein. This represents a hypersensitivity reaction to the measles virus.

bubble_chart Auxiliary Examination

1. Peripheral blood picture: During the stage of full eruption, the white blood cell count often drops to 4,000–6,000/mm³, with a particularly notable decrease in neutrophils.
2. Smear examination for multinucleated giant cells: Nasopharyngeal and ocular secretions, as well as urinary sediment smears stained with Wright's stain, may reveal exfoliated epithelial multinucleated giant cells under microscopy. These can test positive 1–2 days before or after eruption, earlier than the appearance of measles mucous membrane spots (Koplik spots), aiding in early diagnosis.
3. Virological tests: Fluorescent-labeled specific antibodies can detect measles antigen in epithelial cells or white blood cells from nasal mucosal imprints or urinary sediment, with positive results having diagnostic value. Isolation of the measles virus from nasopharyngeal and ocular secretions or blood leukocytes in the early stages confirms the diagnosis. During the convalescence stage, a fourfold or greater increase in serum hemagglutination inhibition and complement-fixing antibodies, or an antibody titer greater than 1:60 one month after onset, supports the diagnosis. Specific IgM measurement also holds value for early diagnosis.

bubble_chart Diagnosis

Based on epidemiological data and clinical manifestations, the diagnosis of typical measles is not difficult. The measles mucous membrane spots are extremely helpful for early diagnosis before the eruption, and the characteristics of upper respiratory catarrhal symptoms and the morphology and distribution of the rash also aid in diagnosis. The post-measles pigmentation and bran-like desquamation during the

stage of convalescence have diagnostic significance. During the stage of full eruption, measles needs to be differentiated from other eruptive diseases, such as:

1. rubella, which has a short prodromal period, mild systemic symptoms, no mucous membrane spots, scattered and slightly pale rashes that fade within 1–2 days, and no pigmentation or desquamation;
2. roseola infantum, which is more common in infants and young children, characterized by sudden high fever for several days and the appearance of rose-colored scattered rashes as the fever subsides;
3. scarlet fever, which presents with fever and sore throat for 1–2 days, followed by a diffuse scarlet rash of pinpoint size with reddened skin between the rashes, and large-scale peeling after the rash subsides. Leukocytosis with a predominance of neutrophils is observed, and throat swab cultures may yield group A β-hemolytic streptococci;
4. enterovirus infections, where the rash is nonspecific and may present as maculopapules, vesicles, or petechiae, often accompanied by sore throat, myalgia, diarrhea, and aseptic meningitis;
5. drug rashes, which often have a recent medication history, exhibit diverse rash patterns, and subside gradually after discontinuation of the drug.

bubble_chart Treatment Measures

No specific antiviral drugs have been discovered for the measles virus to date, so the focus of treatment is on strengthening care, symptomatic management, and preventing complications.

1. **Nursing and Symptomatic Treatment**

Patients should rest in bed and be isolated in a single room. The living space should have fresh air, with appropriate temperature and humidity. Clothing and bedding should not be excessive. The eyes, nose, mouth, and skin should be kept clean. The diet should be nutritious and easy to digest, with plenty of warm water. Avoid dietary restrictions, and additional meals should be provided during the **stage of convalescence**. For high fever, a small **dose** of antipyretics may be given, and cough suppressants can be administered for severe coughing. Weak or severely ill patients may receive early intramuscular injections of gamma globulin or small, frequent transfusions of blood or plasma. Recent reports suggest that supplementing measles patients with vitamin A (100,000–200,000 IU orally in a single dose) can alleviate symptoms and reduce mortality.

2. **Chinese Medicine Treatment**

During the **prodromal stage** (initial fever), **Toxin-Expelling Exterior-Relieving Decoction** or **Cimicifuga and Pueraria Decoction** may be modified to **release the exterior with pungent-cool** herbs and expel pathogens. For external use, **promoting eruption** herbs (15g each of raw **Ephedra**, coriander seeds, **Chinese tamarisk twig**, and purple **Spirodela**) can be boiled in a cloth bag and used for steam inhalation beside the bed or applied to the face and limbs to aid **eruption**. During the **stage of full eruption**, the focus should be on **clearing heat, removing toxins, and promoting eruption**, using **Heat-Clearing Exterior-Expelling Decoction**. For severe cases, **Three Yellow and Gypsum Decoction** or **Rhinoceros Horn and Rehmannia Decoction** may be used. For patients with weakness and cold limbs, **Ginseng Antiphlogistic Decoction** or **Tonifying the Middle and Augmenting Qi Decoction** can be prescribed. During the **stage of convalescence**, **nourishing yin and clearing heat** is recommended, using **Ginseng and Ophiopogon Tuber Decoction** or **Bamboo Leaf and Gypsum Decoction**.

3. **Treatment of Complications**

1. **Pneumonia**: Managed as general pneumonia. For secondary bacterial infections, appropriate antibiotics should be selected. Severe cases may require short-term corticosteroid therapy. Adequate fluid replacement and supportive therapy should be provided for patients with reduced food intake.
2. **Laryngitis**: Maintain humidity in the room and use steam inhalation several times a day to thin mucus. One or two antibiotics should be selected. Severe cases may require oral prednisone or intravenous dexamethasone. Keep the patient calm. If laryngeal obstruction progresses rapidly, tracheal intubation or tracheostomy should be considered early.
3. **Cardiovascular Dysfunction**: In cases of heart failure, **strophanthin-K** or **cedilanid** should be administered early, and **furosemide** may be used for diuresis. Control the total volume and speed of fluid replacement to maintain electrolyte balance. If necessary, an **energy mixture** (coenzyme A, ATP, cytochrome C) and intravenous vitamin C can be given to protect the myocardium. Circulatory failure should be managed as shock.
4. **Encephalitis**: Managed similarly to viral encephalitis, with a focus on symptomatic treatment. Reduce fever in patients with high temperatures and use anticonvulsants for seizures. Strengthen nursing care for **unconscious** patients. Currently, there is no specific treatment for **subacute sclerosing panencephalitis**.

bubble_chart Prognosis

The prognosis of measles is closely related to the patient's immune strength. Young children with weak constitutions, malnutrition, rickets, or other diseases—especially those with compromised cellular immune function—often experience more severe conditions, prolonged recovery, and a higher risk of complications. Inadequate care and deficient treatment can also worsen the illness. Early diagnosis and prompt administration of active or passive immunization can help mitigate the severity of the disease.

bubble_chart Prevention

Enhancing population immunity is the key to preventing measles, so implementing planned immunization for susceptible populations is crucial. If measles patients are identified, comprehensive measures should be taken to prevent transmission and outbreaks.

**I. Active Immunization**

All susceptible individuals should receive the live attenuated measles vaccine. The initial vaccination age should not be less than 8 months, as antibodies from the mother may neutralize the vaccine virus, rendering it ineffective. In China, the initial vaccination is currently scheduled at 8 months, with a booster at 4 years. Other countries recommend the first dose at 15 months for greater safety and suggest that those vaccinated before 1 year of age should receive a booster one year later. The vaccine should be stored in a dark place at 2–10°C. A single subcutaneous injection of 0.2 ml is sufficient, with the same dose for all ages. The best time for vaccination is one month before the measles epidemic season. If susceptible individuals receive emergency measles vaccination within 2 days of exposure to a measles patient, it can still prevent the disease or reduce its severity. If 80% of susceptible individuals are vaccinated during an outbreak, the epidemic can be controlled within 2 weeks. Post-vaccination reactions are mild, with possible low-grade fever for a few days between 5–14 days and occasional sparse, faint red rashes.

Individuals with fever or acute/chronic diseases should delay active immunization. Those with allergic constitutions, active subcutaneous nodules, malignant tumors, leukemia, or those undergoing immunosuppressive therapy, radiation therapy, or with congenital immunodeficiency should not receive the live attenuated measles vaccine. Vaccination should also be postponed for those who have received blood transfusions, blood products, or passive immunization within the past 8 weeks, or other live attenuated viral vaccines within the past 4 weeks, to avoid compromising efficacy.

After receiving the live attenuated measles vaccine, serum antibody levels rise, with a positive rate of 95–98%. Hemagglutination-inhibiting antibodies can appear in the blood as early as 12 days, peaking at 1 month with antibody titers of 1:16 to 1:128. Levels gradually decline over 2–6 months but generally remain at a certain level. In some individuals, antibodies may disappear entirely after 4–6 years, so a booster can be given at ages 4–6. When active immunization coverage in infants exceeds 90%, disease-free zones can be established.

In some countries, the measles vaccine is administered simultaneously with rubella and mumps vaccines without affecting immunization efficacy.

**II. Passive Immunization**

For young, weak, or ill individuals exposed to measles patients, passive immunization within 5 days can prevent the disease, while administration within 5–9 days can only mitigate symptoms. Options include intramuscular injection of gamma globulin (10%) at 0.2 ml/kg, placental globulin at 0.5–1.0 ml/kg, or adult plasma at 20–30 ml. Passive immunity lasts only 3–4 weeks; if re-exposed after 3 weeks, another injection is required.

**III. Comprehensive Preventive Measures**

Upon identifying a measles patient, an epidemic report should be filed immediately, and respiratory isolation should be enforced until 5 days after the rash appears (extended to 10 days if complications arise). Susceptible children exposed to the patient should be quarantined for 3 weeks and given active or passive immunization as appropriate. Those receiving immunizing agents should extend quarantine to 4 weeks. During measles outbreaks, public awareness campaigns should emphasize keeping patients at home, delivering medical care to homes, and keeping susceptible children away from public spaces. Collective institutions should strengthen morning checks and isolate and observe suspected cases.

bubble_chart Complications

Young, weak, malnourished, and immunocompromised individuals are highly susceptible to complications after contracting measles, with the following being common.

(1) Pneumonia: In addition to the measles virus itself causing giant cell pneumonia, secondary pneumonia is prone to occur at various stages of the disease, most commonly during the stage of full eruption. Pathogens often include Staphylococcus aureus, pneumococcus, and adenovirus. When pneumonia complicates the condition, systemic symptoms worsen, with persistent fever, shortness of breath, nasal flaring, cyanosis, and medium to fine moist rales in the lungs. Complications such as empyema, pyopneumothorax, myocarditis, heart failure, and circulatory failure are common. If the disease course is prolonged, it may lead to bronchiectasis. Severe pneumonia is the primary cause of measles-related deaths.

(2) Laryngitis: Measles patients often experience grade I laryngitis, presenting with hoarseness and an irritating dry cough. Severe laryngitis is usually due to bacterial or other viral infections, exacerbating hoarseness. The cough becomes barking, with signs of laryngeal obstruction, hypoxia, cyanosis, and inspiratory dyspnea, accompanied by marked retractions during inspiration. If not promptly treated with moving qi intubation or tracheostomy, it can rapidly progress to grade III laryngeal obstruction, leading to fatal asphyxiation.

(3) Myocarditis and cardiac insufficiency: Severe measles, due to high fever and severe toxic symptoms, can impair myocardial function, especially in malnourished children or those with concurrent pneumonia. Clinical manifestations include pronounced shortness of breath, hypoxia, cold extremities, cyanosis, tachycardia, weak heart sounds, and hepatomegaly. Electrocardiograms show T-wave and ST-segment changes and low voltage. The condition is critical.

(4) Encephalitis: Measles is more likely to cause central nervous system complications than other eruptive diseases, with an incidence of about 1–2%. It typically occurs 2–5 days after eruption, occasionally during the prodromal stage, or 2–3 weeks post-eruption. Early cases may result directly from the measles virus, while advanced cases often involve demyelination of brain tissue, possibly related to immune responses. Symptoms include high fever, limb paralysis, and respiratory failure. Positive meningeal irritation signs are observed, with cerebrospinal fluid cell counts rising to 50–500/mm³, predominantly mononuclear cells, slightly elevated protein, and normal glucose levels. The condition is often critical, with potential sequelae such as spastic paralysis, intellectual impairment, and blindness.

Subacute sclerosing panencephalitis (SSPE): This is a long-term complication of measles, a subacute progressive encephalitis with an incidence of about 1–4 per million. Pathological changes primarily involve degenerative sexually transmitted disease of brain tissue, with measles virus antigens visible in tissue sections, accompanied by eosinophilic inclusions, and the virus can be isolated. Measles antibody levels in blood and cerebrospinal fluid are extremely high (10–40 times higher than in acute measles patients) and remain elevated. Most patients had measles in early childhood, suggesting that the disease may result from the measles virus persisting latently in brain tissue, producing defective viral particles lacking M membrane protein, leading to progressive degenerative brain lesions. Thus, it is now considered a subacute or chronic encephalitis caused by a measles-like virus or measles-related virus. The incubation period ranges from 2 to 17 years, with onset typically in children aged 5–15, more often in boys. The disease begins insidiously, initially manifesting as behavioral abnormalities, intellectual decline, or sleep disturbances and emotional dysphoria. Over weeks or months, symptoms worsen, featuring characteristic myoclonus, intellectual abnormalities, visual and auditory impairments, slurred speech, ataxia, or localized spastic paralysis, progressing to unconsciousness and decerebrate rigidity. The total disease course lasts about a year, ranging from six months to 6–7 years, ultimately leading to death from malnutrition, cachexia, and secondary infections. A hallmark is the dramatic increase in cerebrospinal fluid gamma globulin common bletilla tuber antibody levels, with normal blood and cell counts, and EEG showing irregular high-voltage slow waves.

(5) Others: It can also be complicated by stomatitis, otitis media, and mastoiditis, mostly caused by secondary bacterial infections. Chronic diarrhea, improper care, or dietary restrictions often lead to malnutrition and various vitamin deficiencies. Pre-existing subcutaneous nodule lesions may worsen and spread, developing into millet-sized subcutaneous nodules or nodular meningoencephalitis. After measles, infections such as whooping cough and chickenpox are also prone to occur.