Comparative Parasitology 67(2) 2000 - Peru State College

FUJINO ET AL.—EXPULSION OF ECHINOSTOMES 239
Figure 2. SEM of the control and infected intestinal surface of jirds. a. Control (normal) intestine,
with round villi having regularly arranged microvilli. Scale bar = 5.0 (Jim. b. Intestine infected for 10
days with Echinostoma trivolvis. The intestinal microvilli appear irregularly arranged (arrows) and partly
peeled off (arrowheads). Scale bar = 5.0 fjim.
clined. The number of goblet cells in the control
was 9.6 ± 0.4/VCU. The numbers of mucosal
mast cells were so small that their kinetic changes
were examined in 10 VCU, although the
number of mast cells in infected jirds increased
gradually from 0.2 ± 0.42/10 VCU at day 5 p.i.
to reach a peak of 1.1 ± 0.32/10 VCU at day
10 p.i. and then declined gradually. For comparison
of the cell counts, goblet cell numbers
were multiplied 10 times as for the mast cells.
The numbers of cells were log-transformed to
normalize the data in Figure 1. Fujino et al.
(1993) examined the worm kinetics and intestinal
cytopathology in conventional and congenitally
athymic BALB/c mice and noted that worm
rejection was caused by goblet cell hyperplasia
and not by mast cells.
The SEM observations of the surface of the
intestinal villi infected with E. trivolvis and the
control showed a rough and irregular arrangement
of microvilli in the infected intestine compared
with the regular microvilli arrangement in
the control intestine (Fig. 2). The intestine infected
with worms was partly damaged by day
10 p.i., and its epithelial surface was eroded. The
TEM observations showed that the intestinal epithelium
appeared more electron-dense than that
in the control (not shown). The distal ends of
the villi were partly broken and the microvilli
were partially eroded. Numerous vesicles of various
sizes appeared in the intestinal epithelium.
The appearance of these vesicles was also re-
ported in BALB/c and C3H mice infected with
E. trivolvis by Fujino et al. (1993) and Fujino
and Fried (1993a), respectively. Matrices of
many small rounded mitochondria were granular
and irregularly condensed. Elongate nuclei with
an irregular peripheral margin had heterochromatin
arranged in small patches and randomly
distributed. Fujino and Fried (1996) noted histopathological
differences in mouse versus hamster
small intestine infected with E. trivolvis and
showed no marked histopathological and histochemical
changes in the hamster intestines. They
suggested that the response of the hamster to E.
trivolvis infection was relatively weak and that
this host showed only a limited capacity to expel
E. trivolvis.
Literature Cited
Christensen, N. 0., P. E. Simonsen, A. B. Odaibo,
and H. Mahler. 1990. Establishment, survival
and fecundity in Echinostoma caproni (Trematoda)
infections in hamsters and jirds. Journal of the
Hclminthological Society of Washington 57:104-
107.
Ellerman, J. R., and T. C. S. Morrison-Scott. 1951.
Checklist of Palaearctic and Indian Mammals,
1758 to 1946. British Museum (Natural History),
London, England. 810 pp.
Franco, J., J. E. Huffman, and B. Fried. 1986. In
fectivity, growth, and development of Echinostoma
revolutum (Digenea: Echinostomatidae) in the
golden hamster, Mesocricetus auratus. Journal of
Parasitology 72:142-147.
Fujino, T., and B. Fried. 1993a. Expulsion of Echinostoma
trivolvis (Cort, 1914) Kanev, 1985 and
Copyright © 2011, The Helminthological Society of Washington