Secondary serological response of patients with chronic hepatosplenic suppurative brucellosis
Immunoglobulin M/biosynthesis/blood
Liver Diseases/blood/immunology/microbiology/pathology
Splenic Diseases/blood/immunology/microbiology/pathology
Issue Date: 
American Society for Microbiology
Diaz R, Ariza J, Alberola I, Casanova A, Rubio MF. Secondary serological response of patients with chronic hepatosplenic suppurative brucellosis. Clin Vaccine Immunol 2006 Nov;13(11):1190-1196.
Chronic hepatosplenic suppurative brucellosis (CHSB) is a local reactivation of a previous brucellosis, coursing with an immunoglobulin G (IgG) and IgA secondary immunological response. The observation of two cases of CHSB with an apparent IgM response gave rise to a detailed serological study of three of our patients. We studied the first sample from all three patients and successive samples from two of them. In cases 1 and 2, we found samples with positive IgM lateral flow and IgM enzyme-linked immunosorbent assay results concomitantly with rheumatoid factor (RF); after absorption with anti-RF serum, these results were rendered negative. In patients 2 and 3 the diagnosis of brucellosis was delayed, because none of the test results were initially very significant. However, a clear seroconversion of IgG antibodies was observed in subsequent months; titers of the Brucellacapt and Coombs tests increased in similar ways, although Brucellacapt decreased more rapidly than Coombs, which persisted at high titers for years. In patient 3 a relapse was observed in the fourth year of follow-up, detected by Coombs and also by IgG lateral flow and counterimmunoelectrophoresis (CIEP), although not by the rose bengal, agglutination, or Brucellacapt tests. Serological changes in CHSB may sometimes be mild and are detected mainly by the Coombs test. Brucellacapt does not offer additional information, although IgG lateral flow and CIEP may be of some use. Careful surveillance of titer changes in the Coombs test is the best marker of infection activity. As the disease progresses, an intense IgG response may develop and RF sometimes appears, simulating an IgM response

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