Measles is one of the most common acute respiratory infections in children. It is highly contagious and is characterized clinically by fever, upper respiratory tract inflammation, measles mucosal spots (Koplik’s spots) and generalized maculopapular rash. Since the widespread use of live attenuated vaccine in China in the 1960s, the incidence of measles has declined significantly.
Etiology.
Measles virus belongs to the family Paramyxoviridae and is spherical particles, about 100-250 nm in diameter, with six structural proteins; measles virus can be isolated in nasal secretions, blood and urine during the prodromal and rash periods. When cultured in human embryos or monkey kidney tissue for 5-10 days, the cells show pathological changes and multinucleated giant cells with intranuclear eosinophilic inclusion bodies are seen. Measles virus has only one serotype and is antigenically stable. The virus is not heat resistant and is sensitive to sunlight and disinfectants, but can be stored for long periods at low temperatures.
Epidemiology.
Patients with measles are the only source of infection, and affected children are infectious from 7 days after exposure to measles to 5 days after rash emergence. The virus is present in the secretions of the conjunctiva, nose, mouth, pharynx, and trachea, and is transmitted by droplets through sneezing, coughing, and talking. The disease is highly contagious, with more than 90% of susceptible persons developing the disease after contact. It used to be prevalent in cities once every 2-3 years, with the highest incidence in children aged 1-5 years. After the use of live attenuated measles vaccine, the incidence has decreased, but the age of onset has shifted because immunity is not durable. The current incidence is more common in unvaccinated preschoolers, immune failed teens, and young adults, and can even form intra-community epidemics.
Infants receive maternal antibodies from the placenta and have passive immunity for 4-6 months after birth, after which they gradually disappear; although maternal antibodies in the blood of the vast majority of infants are undetectable by 9 months of age, some children can persist for up to 15 months, which can interfere with vaccination. Infants of susceptible mothers are not immune to measles and can get the disease before or after delivery.
Pathogenesis.
When a susceptible person inhales nasopharyngeal secretions or droplets containing virus from a measles patient, the measles virus multiplies in the local mucosa for a short period of time, while a small amount of virus invades the blood; thereafter, the virus replicates actively in the mononuclear macrophage system of distant organs and enters the bloodstream in large numbers about the fifth to seventh day after infection, which is the clinical prodromal period. During this period, the virus can be found in tissues such as respiratory epithelial cells and lymphoid tissues, as well as in nasopharyngeal secretions, urine, blood and other secretions and body fluids, and is most infectious at this time. After the appearance of the rash, virus replication decreases, and by day 16 after infection, only the virus in the urine can persist for several days. On the second day after the rash, the serum is almost 100% positive for antibodies and the clinical symptoms begin to improve significantly. The lymphocytes in the cerebrospinal fluid increase significantly in 10% of children, and 50% have electroencephalographic changes at the peak of the disease, but only 0.1% have signs and symptoms of encephalitis, which often appear several days after the acute onset of the disease, when the antibodies in the serum have increased and the virus can no longer be found, so it is considered Autoimmune encephalitis.
Subacute sclerosing holoprosencephalitis, also known as Dawson encephalites. It occurs several years after measles and has been suggested that viral mutations, specific virulence of viral strains or a second viral infection promote the pathogenesis of chronic measles encephalitis, but none of these can be confirmed. Recent studies have revealed that SSPE patients are affected by a blockage in the translation of the M protein (matrix) synthesis in brain cells. Since this protein is necessary for viral assembly, the lack of M protein allows incomplete aggregation of measles virus, which cannot be cleared by antibodies or immune cells, leading to the disease.
Pathology.
Measles is a systemic disease with pathologic changes that can occur in all systems of the body, with the reticuloendothelial system and respiratory system being the most pronounced. The systemic lymphatic system appears hyperplastic, with multinucleated giant cells seen in the lymph nodes, tonsils, liver, spleen, and thymus. Mononuclear cell hyperplasia and multinucleated giant cells surrounding capillaries were seen in the skin, ocular conjunctiva, nasopharynx, bronchi, intestinal mucosa, and especially the appendix, with hypertrophy of lymphoid tissue. Inflammation of microsecretory glands in the submucosa of the buccal mucosa, with plasmacytic exudate and endothelial cell proliferation forming Koplik’s spots within the lesions.
Interstitial pneumonia due to measles is Hecht’s giant cell pneumonia, whereas bronchopneumonia is a secondary bacterial infection. mild inflammation of the meninges is seen in the early stages of SSPE lesions, with total encephalitis involving the cortical and subcortical gray and white matter, surrounded by plasma cells and lymphocytes around the vessels, and glial cells are often proliferating. In the later stages of the disease, there is neuronal degeneration, neuronal loss and myelin loss, and intranuclear inclusion bodies are seen in the nuclei of neurons and stellate cells. Under electron microscopy, the inclusion bodies are tubular in structure and are typical of the paramyxovirus nuclear capsid. These damages are not uniformly distributed in the brain and the changes are inconsistent in the early and late stages of the disease, so brain biopsy is not diagnostic.
Clinical manifestations.
(a) Typical measles can be divided into the following four phases
1. Incubation period.
Generally 10 to 14 days, but also as short as about 1 week. During the incubation period there may be a mild increase in body temperature.
2, the prodromal phase.
Called pre-rash, usually for 3-4 days.
The main manifestations of this period are similar to the symptoms of upper respiratory tract infection.
① Fever, seen in all cases, mostly moderate or above.
(ii) Cicatricial symptoms such as cough, runny nose, lacrimation, and pharyngeal congestion, highlighted by ocular symptoms, conjunctival inflammation, eyelid edema, increased tearing, photophobia, and a distinct congested horizontal line at the edge of the lower eyelid (Stimson’s line), which is extremely helpful in diagnosing measles.
(iii) Koplik’s spots, which appear 24 to 48 hours before the onset of the rash, are small grayish-white dots about 1.0 mm in diameter with a red halo outside, and are seen at first only on the buccal mucosa opposite the lower molars, but they increase quickly within a day and can involve the entire buccal mucosa and spread to the lip mucosa, and the mucosal rash fades away after the rash appears There may be dark red dots left.
(iv) Occasional cutaneous urticaria, vague maculopapular rash or scarlet fever-like rash, which disappears at the appearance of the typical rash.
⑤ Some cases may have some non-specific symptoms, such as general malaise, loss of appetite, and lack of mental energy. Infants may have digestive system symptoms.
3. Rash period.
Most of the rash appears 3~4 days after the fever. The body temperature may suddenly rise to 40~40.5℃, the rash starts as a sparse irregular red papule with normal skin between the rash, starting from behind the ear, neck, along the edge of the hairline, developing downward within 24 hours, spreading over the face, trunk and upper limbs, the rash involves the lower limbs and feet on the third day, the rash is often fused in severe cases, the skin is edematous and the face is puffy and deformed. Most of the rash discolors when pressed, but petechiae may also appear. Lymph node enlargement and splenomegaly are present throughout the body and persist for several weeks, and mesenteric lymph node swelling may cause abdominal pain, diarrhea, and vomiting. Measles pathological changes in the mucosa of the appendix can cause symptoms of appendicitis. Delirium, agitation and lethargy are often present in the extreme phase of the disease, especially during hyperthermia, and are mostly transient, disappearing after the fever subsides, and are not associated with subsequent central nervous system comorbidities. At this stage, there are wet rales in the lungs and increased lung texture is seen on X-ray.
4. Recovery period.
The rash starts to subside 3~4 days after the rash appears, and the order of subside is the same as when the rash appears; without the occurrence of comorbidities, other symptoms such as appetite and spirit also improve. After the rash recedes, the skin is left with bran-like flaking and brown pigmentation, which heals in 7-10 days.
(B) other types of measles
1, mild measles.
Most commonly seen in infants who have received gammaglobulin or adult blood injections during the incubation period, or <8 months of age who still have antibodies in their mothers. The fever is low upper respiratory symptoms are mild, measles mucosal spots are not obvious, the rash is sparse, the duration of the disease is about 1 week, no complications.
2. Severe measles.
Fever up to 40 ℃ or more, toxic symptoms are heavy, with convulsions, coma. The rash is fused purple-blue, often with mucosal bleeding, such as rhinorrhea, vomiting, hemoptysis, hematuria, thrombocytopenia, etc., called black measles, may be a form of DIC; if the rash is less, dull color, often poor circulation performance. This type of children with high mortality.
3, no rash type measles.
Those who have been injected with live attenuated measles vaccine may have no typical mucosal spots and rash, or even no rash appears throughout the course of the disease. This type is not easy to diagnose, only dependent on the prodromal symptoms and serum measles antibody titers increased to confirm the diagnosis.
4. Heterotypic measles.
Caused by inactivated vaccination. The manifestations are high fever, headache, myalgia, no oral mucosal spots; rash from the distal extremities to the trunk, face, polymorphic; often accompanied by edema and pneumonia. Inactivated measles vaccine is not used in China, so this type is rare.
5, adult measles.
Due to the application of measles vaccine, the incidence of measles in adults has gradually increased, differing from that in children: a high incidence of liver damage; gastrointestinal symptoms are common, such as nausea, vomiting, diarrhea and abdominal pain; skeletal myopathy, including joint and back pain; measles mucosal spots exist for a long time, up to 7 days, eye pain is common, but photophobia is rare.
Complications.
(a) Laryngitis, tracheitis, and bronchiolitis.
Measles virus itself can cause inflammation of the entire respiratory tract. Because of the narrow laryngeal cavity, rich vascularity of the mucosal layer, and flaccid connective tissue in children <3 years of age, tracheotomy may be required for airway obstruction if secondary bacterial or viral infection occurs. Clinical manifestations include hoarseness, barking cough, inspiratory dyspnea and trismus, and in severe cases, death by asphyxiation.
(ii) Pneumonia.
Interstitial pneumonia caused by measles virus often subsides after rash and temperature decline. Bronchopneumonia is more common as a result of bacterial secondary infection, the common causative agents are Streptococcus pneumoniae, Streptococcus, Staphylococcus aureus and Haemophilus influenzae, etc., so it is easy to complicate pus or pneumothorax. AIDS patients combined with measles pneumonia, accompanied by a rash, often fatal.
(iii) Myocarditis.
Less common, but transient electrocardiographic changes are common.
(iv) Neurological.
1. measles encephalitis.
The incidence is about 1‰~2‰, mostly fever again 2-5 days after rash, peripheral blood leukocytosis; symptoms such as altered consciousness, convulsions, and sudden coma appear. Cerebrospinal fluid changes are: mild mononuclear cells and protein increase; sugar is normal. The death rate is 10%-25%; 20%-50% of survivors have motor, intellectual or psychiatric sequelae.
2. Subacute sclerosing holoprosencephalitis.
It is a delayed complication of acute infection, manifesting as a progressive decline in brain function, with an incidence of about one in a million; a history of typical measles several years before the appearance of neurological symptoms, and complete recovery. 85% of the onset of the disease at the age of 5-15 years, the beginning of symptoms are very insidious, with mild behavioral changes and learning disabilities, followed by mental retardation, and the appearance of symmetrical, repetitive myoclonus, with intervals of 5-10 seconds; with As the disease progresses, myoclonus disappears and various other abnormal motor and neurological dysfunctions appear, including ataxia, retinal ice, optic nerve atrophy, etc.; finally, it progresses to xylopia, coma, autonomic dysfunction, and decerebrate tonicity. The course of the disease varies, with most patients dying l to 3 years after diagnosis and individuals surviving for more than 10 years.
3. Other.
Geba syndrome, hemiparesis, cerebral thrombophlebitis and retrobulbar optic neuritis are rare.
(v) Deterioration of tuberculosis.
It is not uncommon for children with measles to have a temporarily suppressed immune response and a delayed cutaneous hypersensitivity reaction to tuberculin that can last for several weeks, causing the original latent tuberculosis lesions to become active or even disseminated, resulting in cornual tuberculosis or tuberculous meningitis.
(vi) Malnutrition and vitamin A deficiency.
The process of measles due to high fever and loss of appetite can make the child’s nutritional status become poor and thin; vitamin A deficiency is common, the cornea is cloudy and soft, and develops extremely rapidly, eventually leading to blindness.
Treatment.
(i) General treatment.
Rest in bed, maintain proper temperature and humidity in the room, soft light in the room when there are photophobic symptoms; give easily digestible nutritious food and adequate amount of water; keep the skin and mucous membranes clean.
(B) Symptomatic treatment.
Small amounts of antipyretics are available for high fever; sedatives such as phenobarbital can be given for irritability; cough expectorants are used for severe cough; antibiotics can be given for secondary bacterial infections. Children with measles have a high need for vitamin A. The World Health Organization recommends that children with measles in vitamin A deficient areas should be supplemented with vitamin A.
Prevention.
(i) Passive immunization.
Immune serum globulin 0.25 ml/kg given immediately within 5 days after exposure to measles can prevent the onset of measles; 0.05 ml/kg can only reduce symptoms; more than 6 days will not achieve these results. The clinical course of those who have used immune serum globulin is highly variable, the incubation period is long, and the symptoms and signs are atypical but still potentially infectious to those in contact. Passive immunization can only be maintained for 8 weeks, after which active immunization measures should be taken.
(ii) Active immunization.
The use of live attenuated measles vaccine is an important measure to prevent measles, and its preventive effect can reach 90%. Although mild reactions such as fever, malaise and weakness may occur in 5%-15% of vaccinated children, and a few may develop a rash after fever, there are no secondary bacterial infections and no neurological complications. In China, the age of first vaccination is set at 8 months. If the vaccine is applied too early, the mother’s antibodies remaining in the infant’s body will neutralize the immunizing effect of the vaccine. Because the seropositivity rate after immunization is not l00%, and the immune effect can be weakened over time, the American Advisory Committee on Immunization proposed in 1989: children aged 4-6 years should receive a second measles vaccination when they enter kindergarten or elementary school; young people entering college should be immunized against measles again. People with acute tuberculosis infection should be treated for tuberculosis at the same time if measles vaccination is needed.
(C) Control the source of infection.
Early detection of patients, early isolation. General patient isolation to 5 days after the rash, combined with pneumonia extended to 10 days. Susceptible persons exposed to measles should be quarantined and observed for 3 weeks.
(iv) Cut off the transmission route.
Patient clothing should be exposed to the sun; patients have lived in rooms should be ventilated and irradiated with ultraviolet light, the epidemic season to do a good job of publicity, susceptible children go to public places as little as possible.