Rapid expulsion of the intestinal trematodes Echinostoma trivolvis and E. caproni from C3H/HeN mice after infection with Nippostrongylus brasiliensis.

The number of goblet cells in the small intestines of C3H/HeN mice increased rapidly following their infection with about 500 third-stage larvae (L3) of the intestinal nematode Nippostrongylus brasiliensis. The number of goblet cells reached its peak on day 9 postinfection (p.i.). Worm burdens in the hosts' small intestines were determined following a challenge infection with encysted metacercariae of the intestinal trematodes Echinostoma trivolvis or E. caproni on days 8 and 16 after primary infections with N. brasiliensis. All metacercariae of E. trivolvis or E. caproni used to challenge the hosts on day 8 p.i. were expelled. Considerable numbers of E. trivolvis (48.6%) and E. caproni (67.1%) remained in the intestines of hosts challenged with these echinostomes on day 16 p.i. All the controls used for E. trivolvis and E. caproni infections without primary infections with N. brasiliensis showed recovery rates greater than 70%. An enzyme-linked immunosorbent assay (ELISA) showed that the IgM titer rose remarkably and plateaued on day 11 p.i. No marked rise in the IgG or IgA titer occurred during the experiment. These results indicate that mucins increased by hyperplastic goblet cells associated with primary infections with N. brasiliensis are responsible for a rapid expulsion of the worms of the challenge infection with E. trivolvis or E. caproni from the mouse host.

Fisher syndrome after Campylobacter jejuni enteritis: human leukocyte antigen and the bacterial serotype.

We describe two children who had Fisher syndrome subsequent to Campylobacter jejuni enteritis. The C. jejuni isolates from both patients, who lived in different areas, belonged to PEN 2: LIO 4. One patient had the following human leukocyte antigens (HLAs): HLA-A24, 33; B44, 52; DQ1; and DR2, 6 antigens. Another had the HLA-A24, 33; B44, 54; Cw1; DQ1, 4; and DR4, 6. An effort should be made to isolate C. jejuni from patients with Fisher syndrome and to perform HLA typing so that the pathogenesis of this syndrome can be clarified.