Background

Measles virus in an enveloped single-stranded RNA virus with hemagglutinating and fusion glycoproteins.

 

1. If the patient needed to be admitted, what isolation would be appropriate?

Negative-airflow respiratory isolation. The virus is transmitted by inhalation via large droplet aerosols or by airborne spread. The highest attack rates have been in childhood, usually sparing infants less than 6 months of age because of passively acquired antibody; however, a shift in age-specific attack rates to greater involvement of adolescents and young adults was observed in the United States in the 1980s. This shift is believed to be attributable to the influence of immunization: younger children may be better immunized to limit spread of the virus, whereas older age groups may have missed effective immunization or earlier infection by the wild virus. A marked decline in measles in the early 1990s may reflect decreased transmission as increased immunization coverage takes effect. In the first half of 1993 only 167 cases were reported by US health departments compared to 13,787 during the same months of 1900, a 99% decrease.

Epidemics tend to occur during the winter and spring in 1- to 3-year cycles and increasingly are limited to one dose vaccine failures or groups who do not accept immunizations. The infection rate among exposed susceptible subjects in a classroom or household setting is estimated at 85%, and more than 95% of those infected become ill. The period of communicability is estimated to be 3 to 5 days before appearance of the rash to 4 days afterward.

 

 

 

 

 

 

 

 

 

2. What is known about the pathogenesis of the infection?

After implantation in the upper respiratory tract, viral replication proceeds in the respiratory mucosal epithelium. The effect within individual respiratory cells is profound. Even though measles does not directly restrict host cell metabolism, susceptible cells are damaged or destroyed by virtue of the intense viral replicative activity and the promotion of cell fusion with formation of syncytia. This results in disruption of the cellular cytoskeleton, chromosomal disorganization, and the appearance of inclusion bodies within the nucleus and cytoplasm. Replication is followed by viremic and lymphatic dissemination throughout the host to distant sites, including lymphoid tissues, bone marrow, abdominal viscera, and skin. Virus can be demonstrated in the blood during the first week after illness onset, and viruria persists for up to 4 days after the appearance of rash. During the viremic phase, measles virus infects T and B lymphocytes, circulating monocytes and polymorphonuclear leukocytes without producing cytolysis. The effect of B lymphocytes has been shown to suppress immunoglobulin synthesis; in addition, generation of natural killer cell activity appears to be impaired. There is also evidence that the capability of polymorphonuclear leukocytes to generate oxygen radicals is diminished, perhaps directly by the virus or by activated suppressor T cells. This may further explain the enhanced susceptibility to bacterial superinfections. In addition, virion components can be detected in biopsy specimens of Koplik's spots and vascular endothelial cells in the areas of skin rash.

 

 

 

 

 

 

 

 

 

3. List the clinical signs that the physician focused on to make an accurate clinical diagnosis of measles. What test could be done to confirm the diagnosis?

 


Clinically, measles is usually so characteristic that it is rarely necessary to perform laboratory tests to make a diagnosis. Measles virus is difficult to isolate and grow. The virus can be grown in primary human or monkey cell cultures. Respiratory tract secretions, urine, blood, and brain tissue are recommended specimens. Respiratory and blood specimens are best collected during the prodromal stage up to 1 to 2 days after the appearance of the rash.

Antibody, especially IgM, can be detected when the rash is present and is the best means to confirm the diagnosis.

 

 

 

 

 

 

 

 

 

4. Describe the vaccine that is available to prevent this infection. Why wasn=t this child vaccinated?

Vaccine coverage in many developing countries (such as Mexico) is poor, and the child is at about the usual age for vaccine.

A live attenuated measles vaccine in use since 1963 has significantly reduced the incidence of measles in the United States. The current Schwartz or Moraten attenuated strains of the original Edmonston B vaccine are currently being used in the United States. Live attenuated vaccine is given to all children after 12 months of age, in combination with mumps and rubella vaccine (MMR vaccine). Although successful results are greater than 95%, revaccination is being suggested for children before grade school or junior high school. (A killed measles vaccine, introduced in 1963 and subsequently discontinued, provided only short-term immune protection. Recipients of killed vaccine were at risk for the more serious atypical measles presentation upon infection).

Hospitals in areas experiencing endemic measles may wish to vaccinate or check the immune status of their employees to decrease the risk of nosocomial transmission.

 

 

 

 

 

 

 

 

 

5. Are there any effective anti-viral agents that act against this virus? What is the appropriate treatment? Should any therapy be prescribed for the 4 month old cousin?

Exposed susceptible individuals who are immunocompromised and <2 year old infants should be given immune serum globulin to modify their measles infection. This product is most effective if given within 6 days of exposure. [Babies <2 year old are at a higher risk for development of SSPE (subacute sclerosing panencephalitis)] There are no effective anti-viral agents. Treatment is supportive only.

 

 

 

 

 

 

 

 

 

6. Are there any long term consequences associated with this viral infection?

Subacute sclerosing panencephalitis (SSPE) is an extremely serious, very late neurological sequelae of measles that occurs in about 7 in 1,000,000 patients. In SSPE a defective measles virus persists in the brain and acts as a slow virus. The virus can replicate and spread directly from cell to cell but is not released. Many months or years after clinical measles the patient develops changes in personality, behavior, and memory. Myoclonic jerks, blindness and spasticity follow. Unusually high levels of measles antibodies are found in the blood and spinal fluid. Eosinophilic inclusion bodies composed of paramyxovirus-like nucleocapsids are present in the brains of patients with SSPE. The incidence of SSPE has decreased markedly with the success of measles vaccination.

SSPE does not occur with immunization.