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Current Trends Serologic Diagnosis of Measles

As the countdown for measles elimination has progressed, increasing efforts have been made to confirm measles cases by laboratory methods. As an additional measles serodiagnostic test, a staphylococcal protein A (SPA) adsorption test has recently been adapted to measure measles-specific IgM (1,2). This test is based on the principle that SPA will bind IgG antibody and will permit its removal from a serum specimen, allowing any residual measles IgM antibody to be measured by routine hemagglutination-inhibition (HI) testing (3).

The sensitivity and specificity of the SPA test were assessed relative to sucrose gradient ultracentrifugation (SGU), the standard method for measuring measles-specific IgM, using 79 serum specimens from patients clinically suspected of having measles (Table 1) (4). The sensitivity of the SPA was 71% (45/63), and the specificity was 81% (13/16). In this study, a positive IgM detected by SPA was almost always confirmed as IgM by the SGU; of the 48 serum specimens positive by SPA, 45 (94%) were also positive by SGU. However, a negative SPA test did not mean IgM was absent; of the 31 specimens that tested negative by the SPA test, 18 (58%) were positive by SGU.

Serum specimens from 36 measles cases confirmed by a four-fold or greater rise in complement-fixation or HI-antibody titer were used to determine when measles IgM becomes positive by SPA. Only six of 19 (32%) specimens collected 0-4 days after rash onset were positive by SPA compared with 12 of 17 (71%) specimens collected 5-21 days following rash onset (X((2)) = 4.01, p = 0.045). Reported by Viral Exanthems and Herpes Virus Br, Div of Viral Diseases, Center for Infectious Diseases, Surveillance, Investigations, and Research Br, Immunization Div, Center for Prevention Svcs, CDC.

Editorial Note

Editorial Note: The techniques most commonly used to confirm measles infections serologically are the HI and the complement-fixation (CF) tests (3). A four-fold rise in measles-specific HI or CF antibody titers between acute- and convalescent-phase serum specimens confirms measles infection. HI antibodies generally become detectable within the first several days following rash onset and peak approximately 2 weeks later (Figure 1) (5-7). Complement-fixation titers frequently follow the rise in HI titers, often by 1-3 days. However, there is considerable individual variation; some persons reach peak HI and CF titers within the first few days after rash onset (5,8,9). Measles-specific IgM antibodies may be detected shortly after rash onset and peak within 10 days after rash onset; they are usually undetectable by 30 days (10).

The SGU method (used most often to measure measles IgM) is cumbersome and time-consuming and requires expensive and sophisticated equipment. The SPA adsorption test, although less sensitive than SGU for detecting IgM, is simple to perform and requires the addition of only one adsorption step to the serum-treatment procedure for the measles HI assay. Laboratories that perform the HI assay should consider adding the SPA technique for IgM measurement and should establish internal quality control with known IgM positive and IgM negative specimens. A positive test is presumptive evidence of acute measles infection. The three instances in which the SPA adsorption test was positive and the SGU was negative may have been false positives. However, it is possible that the SPA adsorption test may have detected IgM not detectable by SGU. A negative SPA adsorption test, however, should not be interpreted as the absence of IgM.

The laboratory is more helpful for confirming measles cases than for ruling out measles as the cause of a rash illness. The presence of measles-specific IgM or the detection of a four-fold rise in measles HI or CF antibody titers between acute- and convalescent-phase serum specimens confirms an acute measles infection. However, IgM may not be detected, even in specimens collected when antibody should peak, and four-fold rises may go undetected, particularly if peak titers were reached before an acute-phase specimen was drawn (11).

Laboratory confirmation should be sought for all suspected cases of measles occurring in the United States. However, decisions to take outbreak-control measures should be made on clinical and epidemiological grounds, since laboratory confirmation may take several weeks from rash onset, and the absence of laboratory evidence for measles infection may not rule out measles.


  1. Herrmann KL. Prospects for a more rapid and accurate test for measles. In: Proceedings of the 16th Immunization Conference, May 18-21, 1981. Atlanta: Centers for Disease Control 1981:53-4.

  2. Ankerst J, Christensen P, Kjellen L, Kronvall G. A routine diagnostic test for IgA and IgM antibodies to rubella virus: adsorption of IgG with Staphylococcus aureus. J Infect Dis 1974;130:268-73.

  3. Gershon AA, Krugman S. Measles virus. In: Lennette EH, Schmidt NJ, eds. Diagnostic procedures for viral, rickettsial and chlamydial infections, 5th ed. Washington, DC: American Public Health Association 1979.

  4. Vesikari T, Vaheri A. Rubella: a method for rapid diagnosis of a recent infection by demonstration of the IgM antibodies. Br Med J 1968;1:221-3.

  5. Krugman S, Giles JP, Friedman H, Stone S. Studies on immunity to measles. J Pediatr 1965;66:471-88.

  6. Cutchins EC. A comparison of the hemagglutination-inhibition, neutralization and complement fixation tests in the assay of antibody to measles. J Immunol 1962;88:788-95.

  7. Enders-Ruckle G. Methods of determining immunity, duration and character of immunity resulting from measles. Arch Ges Virusforsch 1965;16:182-207.

  8. Stokes J Jr, Reilly CM, Buynak EB, Hilleman MR. Immunologic studies of measles. Am J Hyg 1961;74:293-303.

  9. Bech V. Studies on the development of complement fixing antibodies in measles patients. Observations during a measles epidemic in Greenland. J Immunol 1959;83:267-75.

  10. Black FL. Measles. In: Evans AS, ed. Viral infections of humans. Epidemiology and control. New York: Plenum Medical Book Company 1976:297-316.

  11. Cherry JD, Feigin RD, Shackelford PG, Hinthorn DR, Schmidt RR. A clinical and serologic study of 103 children with measles vaccine failure. J Pediatr 1973;82:802-8.

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