Primary humoral antibody response to Coxiella burnetii, the causative agent of Q fever

Guigno, D; Coupland, Ben; Smith, E.G.; Farrell, I. D.; Desselberger, Ulrich; Caul, E.O.

doi:10.1128/jcm.30.8.1958-1967.1992

Cited by 49 publications

(23 citation statements)

References 22 publications

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“…For example, Meurman et al, (1992) found that IgG antibody avidity in patients with respiratory syncytial virus infection can serve to distinguish between primary infection and reinfections. Secondary immune responses generate antibodies of higher avidity, Guigno et al, (1992) reported that IgG antibody avidity to Coxiella burnetii, the causative organism of Q fever, changed significantly when the time elapsed after infection is considered, Joynson et al, (1990) reported that patients with acute toxoplasmosis infection had low avidity IgG antibody while patients with chronic infection showed high avidity antibody. Consequently, analysis of antibody avidity to periodontal pathogens may help distinguish between acute exacerbations and quiescent periods of the disease.…”

Section: Discussionmentioning

confidence: 99%

Serum IgG antibody response to Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis: implications for periodontal diagnosis

Lamster

Kaluszhner-Shapira

Herrera‐Abreu

et al. 1998

J Clinic Periodontology

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The relationship of the serum antibody titer and avidity to the putative periodontal pathogens Actinobacillus actinomycetemcomitans (Aa) strains Y4 and 29523 and Porphyromonas gingivalis (Pg) strain 381 were examined in relation to clinical parameters in 26 gingivitis and 28 periodontitis patients. The relationship of antibody titer and avidity to infection with the homologous organism was also examined in a subset of 30 patients. Antibody titer was determined by an enzyme-linked immunosorbent assay, and antibody avidity was assessed using a dissociation assay. Considering all patients, there was a significant negative correlation between mean probing depth and antibody titer (r=-0.28) and avidity (r=-0.28) to Aa Y4. There was a significant positive correlation of probing depth and antibody titer (r=0.46) and avidity (r=0.46) to Pg. The correlation of antibody titer and avidity to Aa and infection with Aa Y4 (r=-0.32, r=-0.21) and Aa 29523 (r=-0.35, r=-0.39) was negative, while the correlations of titer and avidity to Pg and presence of the organisms was strongly positive (r=0.40, r=0.35). These data indicate that the relationship of serum antibody titer and avidity to clinical parameters of periodontal disease severity and the level of infection with the homologous organism appears to be different for Aa and Pg. The development of an antibody response to Aa appears to protect the individual from infection with the organism. In contrast, the development of an antibody response to Pg was not able to eliminate the infection. These results should be considered when developing a diagnostic strategy for periodontal disease utilizing the humoral immune response.

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Section: Discussionmentioning

confidence: 99%

Serum IgG antibody response to Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis: implications for periodontal diagnosis

Lamster

Kaluszhner-Shapira

Herrera‐Abreu

et al. 1998

J Clinic Periodontology

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“…Heat-inactivated sera were tested against either phase I or phase II C. burnetii antigens (147). A complement fixation anti-phase II antibody titer of Ն40 indicated a diagnosis of acute Q fever (126), whereas an anti-phase I antibody titer of Ͼ200 indicated a diagnosis of chronic Q fever (273). The complement fixation test is specific but has a lower rate of sensitivity and is more time-consuming than IFA or ELISA (270).…”

Section: Serologymentioning

confidence: 99%

“…The complement fixation test is specific but has a lower rate of sensitivity and is more time-consuming than IFA or ELISA (270). Moreover, seroconversion is detected by complement fixation at a later date: 2 to 3 weeks for the complement fixation test, compared to 10 to 15 days for IFA and ELISA (126,270). In addition, false-negative results have been described with the complement fixation test in chronically infected patients with high antibody titers due to a prozone phenomenon, as well as false-positive results due to crossreactions with hen egg antigens.…”

Section: Serologymentioning

confidence: 99%

Q Fever

1999

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SUMMARY Q fever is a zoonosis with a worldwide distribution with the exception of New Zealand. The disease is caused by Coxiella burnetii, a strictly intracellular, gram-negative bacterium. Many species of mammals, birds, and ticks are reservoirs of C. burnetii in nature. C. burnetii infection is most often latent in animals, with persistent shedding of bacteria into the environment. However, in females intermittent high-level shedding occurs at the time of parturition, with millions of bacteria being released per gram of placenta. Humans are usually infected by contaminated aerosols from domestic animals, particularly after contact with parturient females and their birth products. Although often asymptomatic, Q fever may manifest in humans as an acute disease (mainly as a self-limited febrile illness, pneumonia, or hepatitis) or as a chronic disease (mainly endocarditis), especially in patients with previous valvulopathy and to a lesser extent in immunocompromised hosts and in pregnant women. Specific diagnosis of Q fever remains based upon serology. Immunoglobulin M (IgM) and IgG antiphase II antibodies are detected 2 to 3 weeks after infection with C. burnetii, whereas the presence of IgG antiphase I C. burnetii antibodies at titers of ≥1:800 by microimmunofluorescence is indicative of chronic Q fever. The tetracyclines are still considered the mainstay of antibiotic therapy of acute Q fever, whereas antibiotic combinations administered over prolonged periods are necessary to prevent relapses in Q fever endocarditis patients. Although the protective role of Q fever vaccination with whole-cell extracts has been established, the population which should be primarily vaccinated remains to be clearly identified. Vaccination should probably be considered in the population at high risk for Q fever endocarditis.

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“…The interpretation of results requires acute-and convalescent-phase serum samples. Seroconversion is detected later by the complement fixation test than by the immunofluorescence assay or ELISA (between 10 and 20 days after the onset of symptoms) (57,134).…”

Section: Specific Laboratory Diagnosismentioning

confidence: 99%