The World Health Organization WHO recommends the collection of rubella virus genotype data to support global control and elimination programs. In order to facilitate the use of virologic surveillance in these programs, WHO established a systematic nomenclature for wild-type rubella viruses pdf icon external icon see page in The classification of a rubella virus requires sequencing of nucleotides nt in the E1 protein coding region nts and a phylogenetic comparison of the resulting sequence with 32 well-characterized reference virus sequences that represent the 13 genotypes.
In addition, a naming convention exists pdf icon external icon see page based on whether the sequence is derived from a virus isolate or directly from a clinical specimen, and the location and date of specimen collection.
Currently, four genotypes of rubella virus are known to be commonly circulating in many regions of the world: 1E, 1G, 1J, and 2B. See Molecular Epidemiology section on the References and Resources page for additional information. Skip directly to site content Skip directly to page options Skip directly to A-Z link. The lesions tend to be discrete at first, but rapidly coalesce to produce a flushed appearance. The onset of rash is often accompanied by low-grade fever.
Clinical findings, virus shedding, and serologic response in postnatally acquired rubella. The earliest and perhaps the most prominent and characteristic symptom of rubella infection is lymphadenopathy of the postauricular, occipital, and posterior cervical lymph nodes; this is usually most severe during the rash but may occur even in the absence of rash. Postnatal rubella usually resolves without complication. Other complications of rubella, reported with much less frequency than arthritis, include encephalitis and thrombocytopenic purpura.
Rubella infection acquired during pregnancy can result in stillbirth, spontaneous abortion, or several anomalies associated with the congenital rubella syndrome. The clinical features of congenital rubella vary and depend on the organ system s involved and the gestational age at the time of maternal infection Table The classic triad of congenital rubella syndrome includes cataracts, heart defects, and deafness, although many other abnormalities, as noted in the Table, may be seen.
Defects may occur alone or in combination and may be temporary or permanent. The risk of rubella-associated congenital defects is greatest during the first trimester of pregnancy. Some defects have been reported after maternal infections in the second trimester.
Abnormalities Associated with Congenital Rubella Syndrome. Rubella virus is a spherical to nm, positive-sense, single-stranded RNA virus consisting of an electron-dense to nm core surrounded by a lipoprotein envelope. The virus particles are generally spherical with spiky hemagglutinin-containing surface projections.
Rubella virus is the single member of the genus Rubivirus in the family Togaviridae. It is serologically distinct from other members of the Togaviridae, and, unlike most other togaviruses, is not known to be transmitted by an arthropod. Only one genetically stable serotype of rubella virus has been identified.
Phylogenetic tree analysis of nine virus strains indicate the existence of at least three distinct genetic lineages.
Rubella virus contains three major structural polypeptides: two membrane glycoproteins, E1 and E2 and a single nonglycosylated RNA-associated capsid protein, C, within the virion. One of the envelope proteins, E1, is responsible for viral hemagglutination and neutralization. E2 has been found in two forms, E2a and E2b due to differences in glycosylation.
The differences among strains of rubella viruses have been correlated with differences in the antigenicity of E2. Humans are the only known reservoir of rubella virus, with postnatal person-to-person transmission occurring via direct or droplet contact with the respiratory secretions of infected persons.
Although the early events surrounding infection are incompletely characterized, the virus almost certainly multiplies in cells of the respiratory tract, extends to local lymph nodes, and then undergoes viremic spread to target organs Fig. Subsequent additional replication in selected target organs, such as the spleen and lymph nodes, leads to a secondary viremia with wide distribution of rubella virus.
At this time approximately 7 days after infection and 7 to 10 days before the onset of rash the virus can be detected in the blood and respiratory secretions Fig.
Viremia disappears shortly after the onset of rash; it is also associated with the appearance of circulating neutralizing antibodies. However, virus shedding from the respiratory tract may continue for up to 28 days following the onset of rash. Rubella infection in the first 3 or 4 months of pregnancy provides opportunities during the period of maternal viremia for invasion of the placenta and subsequent fetal infection. Development of infection probably depends upon gestational age.
It has been estimated that the fetus has a 40 to 60 percent chance of developing multiple rubella-associated defects if the mother is infected during the first 2 months of pregnancy, with the risk dropping to 30 to 35 percent during the third month of gestation and 10 percent during the fourth. This difference in both risk for and severity of fetal infection seen with gestational age may be associated with immature host defenses during the first trimester of pregnancy.
During fetal infection, the virus can multiply in and damage virtually any organ system. Pathogenesis of the congenital defects is not fully understood; however, a number of mechanisms have been proposed.
Cell culture studies show that the virus produces chromosomal abnormalities, slows cellular growth rates, and causes cell lysis and death in some cell types; these effects appear capable of producing the characteristic abnormalities of cell structure and function.
In the congenitally infected fetus and infant, virus persistence occurs in the presence of neutralizing antibodies; immunological tolerance does not develop. Postnatal infection rapidly induces a specific immune response which provides lifelong protection against the natural disease. Neutralizing and hemagglutination-inhibiting antibodies appear shortly after the onset of rash and reach maximum levels in 1 to 4 weeks. Specific antibodies persist after infection.
Cell-mediated immunity also develops in convalescence and can be detected for years following infection. When exposed to rubella virus, individuals with neutralizing or hemagglutination-inhibiting antibodies are most often protected.
However, reinfection with rubella virus has been documented in individuals with demonstrated natural immunity and, more commonly, in vaccinees. The vast majority of such reinfections are asymptomatic, detectable only by a boost in antibody titer; however, a few cases of reinfection-associated rash and arthritis have been reported.
Rubella occurs worldwide. There have been no major epidemics in the United States since the licensure of the live attenuated rubella vaccine in However, limited sporadic outbreaks of rubella continue to occur each year, particularly in settings such as schools where susceptible individuals come into close contact. The incidence of infection shows the same prominent seasonal pattern as for other respiratory diseases. The incidence increases in winter, peaks in spring, and then subsides to extremely low levels in summer and fall.
Epidemiologic data suggest that maximum infectivity occurs from 3 days before the onset of rash until 3 days afterward. However, throat swabs from children with rubella have been reported to contain virus from as early as 10 days before the onset of rash to as late as 28 days afterward. In addition, asymptomatic individuals have been reported to transmit rubella. In the prevaccine era, the disease usually affected children 5 to 9 years old. However, because rubella is less contagious than diseases such as measles and varicella, a significant proportion of the population 10 to 15 percent escaped rubella infection in childhood.
Widespread vaccine use has reduced rubella incidence by more than 99 percent overall Fig. However, a greater percentage of cases that do occur are now reported in unvaccinated young adults. In , 48 percent of reported rubella infections were in persons older than 15 years of age. In addition, about 6 to 11 percent of postpubertal women in the United States currently lack serologic evidence of immunity. These data continue to be of concern; such women continue to remain at risk for rubella during pregnancy.
An average of 39 cases per year of congenital rubella were reported to the Centers for Disease Control between and , falling rather dramatically to an average of only 7 cases per year between and A slight resurgence of rubella and congenital rubella was noted in to However, subsequently the reported numbers of cases have been the lowest ever recorded. In infants with congenital rubella, the virus commonly persists during the first year of life and occasionally even longer.
Such infants thus can serve as reservoirs of infection for health care personnel and other contacts. The occurrence of the typical rash and lymphadenopathy may suggest the diagnosis of rubella. Laboratory diagnosis of rubella is typically made by using serologic studies i. The presence of specific IgM antibodies indicates recent rubella infection. Specific IgG antibodies in healthy individuals demonstrate immunity to rubella. Although ribavirin intravenously or by aerosol has been used to treat measles, no formal studies have been conducted, so its efficacy against measles is unproven.
The safest and most successful approach to measles is prevention. Measles vaccine is usually given as the combination measles, mumps, and rubella MMR vaccines. Currently, 2 doses are usually administered, usually at months of age in outbreaks, vaccine can be given after 6 months of age. The second dose is usually given at the start of school, but can be administered sooner. The minimum interval between doses is 1 month.
Measles is one of the most contagious diseases known; it is spread by the airborne route from respiratory secretions from infected individuals. The prodrome is followed by fever and gradual development of rash. Measles is most contagious just before rash onset and during the first few days after the rash appears. The presence of Koplik spots on the buccal mucosa is pathognomonic of measles.
Complications of measles, including pneumonia and encephalitis, occur in roughly 1 per cases; complications and severe measles are more frequent in immunocompromised patients. More common, less severe complications include otitis media and croup. Measles usually occurs in winter and early spring in countries with temperate climates. The incubation period is days, with an average of 10 days.
Worldwide, there were for many years 1 million annual deaths from measle, although this has recently decreased; in , were reported to WHO. Measles is an enormous problem in developing countries, where infections often occur in very young children with immature immune systems, many of whom are also malnourished, which further impairs their immune response to the virus. Live attenuated measles vaccine was licensed in the United States in Prior to that, an estimated , annual cases occurred in the United States.
Between and , there were less than annual cases in the United States. Measles became no longer endemic in the United States; molecular studies showed all cases to be due to imported measles from Europe, Asia, and the Middle East.
Beginning in , an increase in measles began to occur in the United States. Many cases were related to travel in European and Asian countries, where there were many unvaccinated individuals.
The increase in measles therefore was mainly ascribed to the failure of many parents to immunize their healthy infants, mainly from fear that MMR might be a cause of autism. Others refused vaccination, citing philosophical or religious objections. As many of 15 studies worldwide have failed to demonstrate a causal relationship between MMR vaccine and autism. Today, cases of measles are on the increase in the United States, with reported mini-epidemics among unvaccinated and too-young-to-be-vaccinated children.
In , a record cases of measles were reported in 27 states, the highest number of cases in many years. Most of the cases were unvaccinated. Largely due to refusal of parents to immunize their children. In , 11 measles outbreaks in the US were reported by the CDC, and in 23 outbreaks were reported. In December an outbreak began at a large California amusement park, leading to reported measles cases in 7 states, Mexico and Canada.
There were no fatalities, but a number of patients were hospitalized. Measles cases today are mostly ascribed to reluctance of some parents to vaccinate their children for fear of harm from the vaccine, and importations of measles cases from other countries where vaccination is not practiced. Measles in hospitalized patients requires strict isolation with proper hand-washing, gowns, masks, and gloves.
Hospitalized patients should be in a negative pressure room, if possible. Airborne transmission precautions are indicated until 4 days after rash onset in otherwise healthy patients and for the duration of illness in the immunocompromised.
The incubation period is days after exposure. Measles cases should be reported to the local Department of Health. Second doses of measles-containing vaccines should be at least 1 month apart. Healthy child or adult susceptibles should also be immunized. Exposure to measles in the unvaccinated is not a contraindication to immunization; control of epidemics in schools or other institutions is by immunization. During an outbreak, infants as young as 6 months of age can be vaccinated; such children should eventually receive a total of three doses of measles vaccine.
Health care workers should be required to demonstrate proof of measles immunity before being hired. Adverse events after measles vaccine include fever up to Transient thrombocytopenia and anaphylaxis occur rarely. Measles vaccine considered to be extremely safe. Although pre-formed antibodies are useful for passive immunization and play a significant role in preventing recurrent infections, cellular immunity appears more important in host defense against measles than humoral immunity.
In general, CD4 T-cells help to control the virus by secretion of cytokines, whereas CD 8 T-cells directly eliminate cells infected with measles virus. Some CD4 T-cells are also cytotoxic for measles virus infected cells. Unvaccinated patients at high risk to develop severe measles include infants younger than 6 months of age and immunocompromised individuals, such as those with congenital or acquired defects in cellular immunity, as well as children being treated for malignant disease or following transplantation.
Such individuals should receive passive immunization after a recognized exposure. Exposed HIV-infected children should receive passive immunization whether or not they were immunized. Passive immunization is accomplished with Immune Globulin IG within 6 days after exposure. The dose is 0. Passive immunization is not required for healthy household members who have received at least 1 dose of vaccine. Measles disease is the main manifestation of infection with rubeola virus.
Patients with the prodrome of measles have non-specific respiratory symptoms for about 3 days. Koplik spots appear during and following this prodrome. In the next phase, patients complain of influenza-like symptoms, such as fever, cough, conjunctivitis, and coryza.
After a few more days, the typical maculopapular, erythematous, non-pruritic rash begins on the head and face and progresses down the body. Rash first appears behind the ears and on the hairline. The rash, which blanches on pressure, appears last on the extremities, including the palms and soles.
The rash may become confluent, especially on the face and neck.
0コメント