Gregory Sonnen MD
Nancy Henry MD, PhD
Essentials of Diagnosis
General Considerations
Measles vaccine was introduced for commercial use in 1963. From 1963 to 1967, ~900,000 children received the inactivated measles vaccine. The attenuated, live-virus vaccine was introduced in the late 1960s. By 1973, the inactivated vaccine was no longer available. Before 1963, between 200,000 and 600,000 cases were reported annually in the United States. However, even these reports represent only a fraction of the actual case rate. The number of reported cases dropped from 22,231 in 1968 to 1,497 in 1983.
In the mid-1980s a resurgence of reported cases occurred primarily in the preschool population. Nearly 19,000 cases were reported in 1989. The majority of these cases were in vaccine-eligible, unvaccinated preschool children living in urban areas. In the late 1980s and early 1990s several outbreaks occurred among adolescents and young adults, primarily on college campuses. Most of the cases were in patients with a history of receiving only a single dose of the vaccine. Since 1993, < 1,000 cases have been reported per year. This is likely owing to aggressive revaccination efforts. A second measles vaccination is now standard at ages 4–6 years.
Measles virus is communicable for 3–5 days before the outbreak of the rash. It remains communicable up to 4 days after the appearance of rash. Immunocompromised patients can shed virus for an extended period of time. Patients who develop subacute sclerosing panencephalitis do not continue to shed virus.
CLINICAL SYNDROMES
TYPICAL MEASLES
Clinical Findings
The exanthem phase begins ~2 weeks after exposure. The maculopapular rash first appears on the brow and posterior auricular area. It progresses to cover the face and spreads to the distal extremities within 72 h. Large areas of the rash will progress to confluence, then desquamate leaving transient hyperpigmented areas. The rash usually begins to clear on the 3rd or 4th day. The fever peaks on the 2nd or 3rd day of the rash.
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Table 34-1. Measles clinical findings. |
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Measles infection during pregnancy produces significant fetal morbidity and mortality, especially if infection occurs during the first trimester. Measles uncommonly produces severe abdominal pain during the acute febrile phase. Etiologies for this pain can be mesenteric lymphadenitis or appendicitis. Evidence of peritonitis warrants prompt surgical evaluation.
Subacute sclerosing panencephalitis (SSPE) is a rare, late-onset, lethal neurodegenerative sequela of measles infection. It occurs with an incidence of 0.6–2.2 cases/100,000 infections and 1 case/1 million vaccinations. SSPE results from a slowly progressive chronic infection with the virus. SSPE becomes clinically evident an average of 7 years after initial measles exposure. Symptoms include unusual behavior, developmental regression, ataxia, myoclonic jerks, visual impairment, and aphasia. All of these symptoms are progressive, leading ultimately to decorticate rigidity and death, which usually occurs 6–9 months after onset of symptoms. Confirmation of the diagnosis can be made by electroencephalogram, serology, and analysis of the cerebrospinal fluid. Cerebrospinal fluid shows high IgG as does serum. No current therapy is effective.
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BOX 34-1 Complications of Measles |
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BOX 34-2 Treatment of Measles |
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MODIFIED MEASLES
Modified measles occurs in individuals receiving an incomplete live virus vaccination series and subsequently being infected by the natural virus. It can also occur in infants under 9 months owing to the presence of maternally derived antibodies. It is similar to natural measles infection but less severe (see Table 34-1). The prodromal phase may be shorter and less severe. Koplik's spots may be scant or absent. The exanthem rash usually does not progress to confluence, but has a similar duration. Viral isolation is unaffected. All the complications and sequelae of typical measles can occur.
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BOX 34-3 Control of Measles |
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ATYPICAL MEASLES
Atypical measles occurs in some individuals who received the inactivated virus vaccine in the 1960s and were subsequently exposed to the natural virus. These patients have a prodromal phase noted by sudden onset of high fever, headache, myalgia, and abdominal pain (see Table 34-1). Lobar pneumonia with effusion is common. These patients rarely have Koplik's spots. The exanthem phase begins on the 2nd or 3rd day of illness. The maculopapular rash begins on the palms and soles and spreads centrally. It can progress to vesiculation. Urticaria, purpura, and petechiae are common.
Chest radiographs will commonly show lobar consolidation. Acute and convalescent titers and viral culture are useful. The differential diagnosis of this exanthem includes rickettsial disease, meningococcemia, and hemorrhagic fever.
Diagnosis
Diagnosis of measles is usually based on physical findings. Finding Koplik's spots and monitoring the usual progression of the exanthem are helpful clues. An attempt should be made to culture the virus during the febrile course of the illness. Culture can often be technically difficult. Serology should be obtained as well. Confirmation of a diagnosis should be promptly reported to a local government health agency for epidemiologic tracking.
Treatment
Treatment of measles is often supportive. Hospitalization is not warranted unless the patient is dehydrated, in respiratory distress, encephalopathic, or otherwise compromised. Young patients requiring hospitalization (Box 34-2) should receive vitamin A. Recent clinical studies have shown a decrease in morbidity and mortality in patients receiving vitamin A supplementation. Patients of any age may benefit from vitamin A supplementation if their cases are clinically severe. All patients in areas of known vitamin A deficiency (ie, Third World countries) should receive supplementation if measles is endemic to the area.
Immune globulin may be used to protect susceptible contacts of confirmed measles cases. Immune globulin must be used within 6 days of exposure for maximum efficacy. Contacts who received at least one dose of measles vaccine at age ≥ 12 months do not need immune globulin if they are immunocompetent. Candidates for immune globulin would include nonimmunized pregnant women, the immunocompromised, and infants < 1 year of age. Infants < 5 months of age do have passive maternal antibodies if their mother can be confirmed to be measles immune. If maternal immunity is confirmed, these infants do not need immune globulin. If children receive immune globulin, they should not receive measles vaccine for 5 months (if receiving 0.25 cc/kg immune globulin) or 6 months (if receiving 0.5 cc/kg immune globulin).
The live virus vaccine can modify the infection in a nonimmunized person, if given within 72 h of exposure. Clinical response varies. Usual vaccine contraindications apply to the vaccine if used in this modality (see Box 34-2).
Prevention & Control
Measles is highly communicable. Any hospitalized patient suspected of harboring the virus should be in droplet isolation. Good hand washing and appropriate handling of fomites should be observed as well. This isolation should be maintained during the prodromal phase and 4 days from the onset of the exanthem. Children should also be excluded from school and daycare during this period. Isolation may need to be extended in complicated cases. Some immunocompromised patients can shed virus for an extended period.
School quarantine issues are often difficult. Virus is shed and communicable in the prodromal phase. The diagnosis of measles is often not suspect in this phase. The index case may have many contacts before diagnosis. Quarantine issues should be addressed individually and in conjunction with a local government health agency.
Live attenuated measles vaccine should be administered to healthy individuals at two intervals. The first dose is recommended at age 12–15 months. The second dose should be at age 4–6 years. Children who miss the second dose should receive it before age 12 years.
In epidemic conditions, a dose may be given from ages 6 to 11 months. These patients will still need a dose at age 12–15 months and at 4–6 years (Box 34-3).
REFERENCES
American Academy of Pediatrics, Committee on Infectious Diseases: Measles. In Peter G (editor): 1997 Red Book: Report of the Committee on Infectious Diseases, 24th ed. American Academy of Pediatrics, 1997.
Centers for Disease Control and Prevention: Measles–United States, 1996, and the interruption of indigenous transmission. J Am Med Assoc 1997;277:1345.
Cherry JD: Measles. In Feigin RD, Cherry JD (editors): Textbook of Pediatric Infectious Diseases, 3rd ed. Saunders, 1992.
Hussey GD, Klein M: A randomized, controlled trial of vitamin A in children with severe measles. N Engl J Med. 1990;323:160.
PeBenito R et al: Fulminating subacute sclerosing panencephalitis: Case report and literature review. Clin Pediatr 1997;36:149.