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Journal of Clinical Microbiology logoLink to Journal of Clinical Microbiology
. 1992 May;30(5):1287–1290. doi: 10.1128/jcm.30.5.1287-1290.1992

Age-related interference with Chlamydia pneumoniae microimmunofluorescence serology due to circulating rheumatoid factor.

R P Verkooyen 1, M A Hazenberg 1, G H Van Haaren 1, J M Van Den Bosch 1, R J Snijder 1, H P Van Helden 1, H A Verbrugh 1
PMCID: PMC265266  PMID: 1583133

Abstract

Microimmunofluorescence (MIF) serology is commonly used in the diagnosis of chlamydial infections. In the MIF assay, Chlamydia pneumoniae elementary bodies were used to detect C. pneumoniae immunoglobulin G (IgG) and IgM antibodies in paired serum samples from 286 patients with respiratory illnesses. In 69 patients, MIF serology was compared with C. pneumoniae cultures. All C. pneumoniae cultures remained negative. However, 205 (71%) of 286 patients were C. pneumoniae antibody positive and 64 (22%) had MIF test results indicating recent infection; 11 showed a fourfold increase in IgG titer, 18 had IgG titers of greater than or equal to 1:512, and 41 had IgM titers of greater than or equal to 1:16. In 35 (55%) of 64 patients, a recent-infection diagnosis was based on C. pneumoniae IgM antibodies only. However, 78% of C. pneumoniae IgM-positive patients had circulating rheumatoid factor (RF) by rheumatoid arthritis latex assay. RF positivity increased with age. After absorption with anti-human IgG, all C. pneumoniae IgM-positive sera became C. pneumoniae IgM negative in the MIF assay. Twenty-five patients with active rheumatoid arthritis but without respiratory illness were also tested; 14 were C. pneumoniae IgG positive and C. pneumoniae IgM positive as well. Absorption of IgG from these RF-containing sera invariably resulted in disappearance of reactivity in the MIF IgM assay. We conclude that with age the serologic diagnosis of recent C. pneumoniae infection becomes increasingly prone to false-positive results unless sera are routinely absorbed prior to MIF IgM testing.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Bartfeld H. Distribution of rheumatoid factor activity in nonrheumatoid states. Ann N Y Acad Sci. 1969 Dec 10;168(1):30–40. doi: 10.1111/j.1749-6632.1969.tb43092.x. [DOI] [PubMed] [Google Scholar]
  2. Carson D. A., Chen P. P., Fox R. I., Kipps T. J., Jirik F., Goldfien R. D., Silverman G., Radoux V., Fong S. Rheumatoid factor and immune networks. Annu Rev Immunol. 1987;5:109–126. doi: 10.1146/annurev.iy.05.040187.000545. [DOI] [PubMed] [Google Scholar]
  3. Cles L. D., Stamm W. E. Use of HL cells for improved isolation and passage of Chlamydia pneumoniae. J Clin Microbiol. 1990 May;28(5):938–940. doi: 10.1128/jcm.28.5.938-940.1990. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Grayston J. T., Diwan V. K., Cooney M., Wang S. P. Community- and hospital-acquired pneumonia associated with Chlamydia TWAR infection demonstrated serologically. Arch Intern Med. 1989 Jan;149(1):169–173. [PubMed] [Google Scholar]
  5. Grayston J. T., Kuo C. C., Wang S. P., Altman J. A new Chlamydia psittaci strain, TWAR, isolated in acute respiratory tract infections. N Engl J Med. 1986 Jul 17;315(3):161–168. doi: 10.1056/NEJM198607173150305. [DOI] [PubMed] [Google Scholar]
  6. Grayston J. T., Wang S. P., Kuo C. C., Campbell L. A. Current knowledge on Chlamydia pneumoniae, strain TWAR, an important cause of pneumonia and other acute respiratory diseases. Eur J Clin Microbiol Infect Dis. 1989 Mar;8(3):191–202. doi: 10.1007/BF01965260. [DOI] [PubMed] [Google Scholar]
  7. Henle G., Lennette E. T., Alspaugh M. A., Henle W. Rheumatoid factor as a cause of positive reactions in tests for Epstein-Barr virus-specific IgM antibodies. Clin Exp Immunol. 1979 Jun;36(3):415–422. [PMC free article] [PubMed] [Google Scholar]
  8. McCormick J. N., Wojtacha D., Edmond E., Cohen B., Hart H. Do polyclonal rheumatoid factors carry an 'internal image' of cytomegalovirus, Epstein-Barr virus and nuclear antigens? Scand J Rheumatol Suppl. 1988;75:109–116. doi: 10.3109/03009748809096750. [DOI] [PubMed] [Google Scholar]
  9. Milgrom F. Development of rheumatoid factor research through 50 years. Scand J Rheumatol Suppl. 1988;75:2–12. doi: 10.3109/03009748809096732. [DOI] [PubMed] [Google Scholar]
  10. Nurminen M., Leinonen M., Saikku P., Mäkelä P. H. The genus-specific antigen of Chlamydia: resemblance to the lipopolysaccharide of enteric bacteria. Science. 1983 Jun 17;220(4603):1279–1281. doi: 10.1126/science.6344216. [DOI] [PubMed] [Google Scholar]
  11. Osser S., Persson K. Immune response to genital chlamydial infection and influence of Chlamydia pneumoniae (TWAR) antibodies. Eur J Clin Microbiol Infect Dis. 1989 Jun;8(6):532–535. doi: 10.1007/BF01967475. [DOI] [PubMed] [Google Scholar]
  12. Van Renterghem L., Van den Abeele A. M., Claeys G., Plum J. Prevalence of antibodies to Chlamydia pneumoniae in a pediatric hospital population in Belgium. Eur J Clin Microbiol Infect Dis. 1990 May;9(5):347–349. doi: 10.1007/BF01973742. [DOI] [PubMed] [Google Scholar]
  13. Wang S. P., Grayston J. T. Human serology in Chlamydia trachomatis infection with microimmunofluorescence. J Infect Dis. 1974 Oct;130(4):388–397. doi: 10.1093/infdis/130.4.388. [DOI] [PubMed] [Google Scholar]

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