title: Asymptomatic carriage of Clostridium difficile and serum levels of IgG antibody against toxin A.
abstract: BACKGROUND
  Clostridium difficile infection can result in asymptomatic carriage, mild diarrhea, or fulminant pseudomembranous colitis. We studied whether antibody responses to C. difficile toxins affect the risks of colonization, diarrhea, and asymptomatic carriage.
  
  
  METHODS
  We prospectively studied C. difficile infections in hospitalized patients who were receiving antibiotics. Serial stool samples were tested for C. difficile colonization by cytotoxin assay and culture. Serum antibody (IgA, IgG, and IgM) levels and fecal antibody (IgA and IgG) levels against C. difficile toxin A, toxin B, and nontoxin antigens were measured by an enzyme-linked immunosorbent assay (ELISA).
  
  
  RESULTS
  Of 271 patients, 37 (14 percent) were colonized with C. difficile at the time of admission, 18 of whom were asymptomatic carriers. An additional 47 patients (17 percent) became infected in the hospital, 19 of whom remained asymptomatic. The baseline antibody levels were similar in the patients who later became colonized and those who did not. After colonization, those who became asymptomatic carriers had significantly greater increases in serum levels of IgG antibody against toxin A than did the patients in whom C. difficile diarrhea developed (P<0.001). The adjusted odds ratio for diarrhea was 48.0 (95 percent confidence interval, 3.4 to 678) among patients with colonization who had a serum level of IgG antibody against toxin A of 3.00 ELISA units or less, as compared with patients with colonization who had a level of more than 3.00 ELISA units.
  
  
  CONCLUSIONS
  We find no evidence of immune protection against colonization by C. difficile. However, after colonization there is an association between a systemic anamnestic response to toxin A, as evidenced by increased serum levels of IgG antibody against toxin A, and asymptomatic carriage of C. difficile.
authors.affiliation: Division of Gerontology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.
authors.forename: L
authors.initials: L
authors.lastname: Kyne
authors.forename: M
authors.initials: M
authors.lastname: Warny
authors.forename: A
authors.initials: A
authors.lastname: Qamar
authors.forename: C P
authors.initials: CP
authors.lastname: Kelly
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000907:Antibodies, Bacterial / Q000097:blood*; D001426:Bacterial Proteins; D001427:Bacterial Toxins / Q000276:immunology*; D016360:Clostridioides difficile / Q000276:immunology* / Q000302:isolation & purification; D015169:Colony Count, Microbial; D003428:Cross Infection / Q000276:immunology / Q000382:microbiology; D003967:Diarrhea / Q000145:classification / Q000276:immunology / Q000382:microbiology*; D004768:Enterotoxins / Q000276:immunology*; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D011446:Prospective Studies
chemical_list: D000907:Antibodies, Bacterial; D001426:Bacterial Proteins; D001427:Bacterial Toxins; D004768:Enterotoxins; D007074:Immunoglobulin G; C041348:tcdA protein, Clostridium difficile; C031815:toxB protein, Clostridium difficile