Correspondence

Campylobacter jejuni Infection and Guillain–Barré Syndrome

N Engl J Med 1996; 334:802March 21, 1996

Article

To the Editor:

Rees et al. (Nov. 23 issue)1 suggest that Campylobacter jejuni infection has a role in the development of Guillain–Barré syndrome. Their microbiologic and serologic data show evidence of recent C. jejuni infection in 26 percent of their patients with Guillain–Barré or Miller Fisher syndrome, as compared with 2 percent of household controls and 1 percent of age-matched hospital controls. Their study supports several previous case reports and studies of this association. However, we are seriously concerned about the possibility that the serologic diagnosis of C. jejuni infection in some cases of Guillain–Barré syndrome could have led to an overestimate because of the previous administration of intravenous IgG immune globulin for the treatment of these patients.2 In fact, in four patients the diagnosis of C. jejuni infection was based exclusively on the detection of IgG antibodies. The samples for serologic analysis were obtained a mean of 29 days after the onset of symptoms; during this time the patients could have received a large amount of intravenous immune globulin, which would have passively transferred antibodies against C. jejuni. This hypothesis is plausible, since immune globulin is obtained from pooled serum from healthy volunteers, and at least 1 percent of the control patients in this report had serologic evidence of previous infection by C. jejuni. The patients who recovered slowly or had severe residual disability could have received more immune globulin than the patients with a less protracted course of illness, which might explain the association of severe Guillain–Barré syndrome with C. jejuni infection.

Jose M. Aguado, M.D.
Jose T. Ramos, M.D.
Carlos Lumbreras, M.D.
Hospital 12 de Octubre, 28041 Madrid, Spain

2 References

1. 1

   Rees JH, Soudain SE, Gregson NA, Hughes RAC. Campylobacter jejuni infection and Guillain-Barré syndrome. N Engl J Med 1995;333:1374-1379
   Full Text | Web of Science | Medline

2. 2

   van der Meche FGA, Schmitz PIM, Dutch Guillain-Barre Study Group. A randomized trial comparing intravenous immune globulin and plasma exchange in Guillain-Barré syndrome. N Engl J Med 1992;326:1123-1129
   Full Text | Web of Science | Medline

Author/Editor Response

Dr. Rees replies:

To the Editor: Aguado et al. suggest that we may have overestimated the number of patients with C. jejuni infection by detecting anti–C. jejuni antibodies derived from intravenous immune globulin administered before venesection. If treatment with immune globulin was responsible for the presence of high titers of anti–C. jejuni antibodies, then we would have expected to see a significantly higher proportion of C. jejuni–positive patients tested after receiving immune globulin than C. jejuni–negative patients. Fifty-six patients had received immune globulin treatment alone, of whom 19 were positive for C. jejuni. Four of these 19 patients had been given a diagnosis on the basis of stool cultures. Thirteen of the remaining 15 (87 percent), as compared with 31 of 37 C. jejuni–negative patients (84 percent), were tested during or after immune globulin treatment (P = 0.9). Twenty-two of the C. jejuni–negative patients who were tested after immune globulin treatment had no measurable antibodies. In addition, 10 of the 15 C. jejuni–positive patients (67 percent) had reported a preceding diarrheal illness — a criterion for the diagnosis of C. jejuni infection.

In answer to the second point: all but one patient from the cohort received only one course of immune globulin, because their condition did not improve. We therefore dispute the claim that immune globulin treatment is responsible for the subsequent positive results on serologic testing for anti–C. jejuni antibodies.

Jeremy H. Rees, Ph.D., M.R.C.P.
Royal Free Hospital, London NW3 2QG, United Kingdom