In vivo development of Echinostoma malayanum Leiper, 1911 with notes on effects of population density, chemical composition and pathogenicity and in vitro excystment of the metacercaria (Trematoda: Echinostomatidae)

Abstract

In vivo development of Echinostoma malayanum Leiper, 1911 was studied in white rats and the developmental process was arbitrarily divided into four stages: organogeny, vitellogenesis, formation of Mehlis' gland complex and cirrus sac, and oviposition. The percentage of development was 86-94. Population density affected the prepatent period of flukes and the normal prepatent period of 13-16 days was altered to 18-23 days in infection with 500-800 flukes. The majority of flukes in heavy infection were undersized and in the immature stage of development at patency. Data from chemical analysis of flukes revealed that protein, lipids, calcium and ash decreased quantitatively in flukes from higher population densities but no such change was observed as regards glycogen. Pathological changes in the rat intestine included lysis and destruction of mucosa, increased activity of goblet cells, oedematous and reticulated appearance of lamina propria and slight to moderate hyperplasia of epithelial cells. The metacercariae excysted in the medium containing trypsin plus sodium cholate an pepsin, though not essential for a high percentage of excystment, affected the rate. The reductant sodium dithionite substantially enhanced the rate and percentage of excystment. Excystation was optimal at pH 8, and 42 degrees C was more effective than 39 degrees C.

The effects of crowding on adults of Echinostoma caproni in experimentally infected golden hamsters

“…RANKIN (1937) noted the relationship between number and size of trematodes within a host and suggested that crowding may be the factor involved. Other reports on crowding with intestinal trematodes include those by WILLEY (1941), FRIED & NELSON (1978), MOHANDAS & NADAKAL (1978), FRIED & FREEBORNE (1984) and FRANCO et al (1988). MOHANDAS & NADAKAL (1978) have shown retarded growth of Echinostoma malayanum at high parasite densities.…”

Echinostomes as Experimental Models for Biological Research

“…Rankin (1937) noted the relationship between number and size of trematodes within a host and suggested that crowding may be the factor involved. Mohandas and Nadakal (1978) have shown retarded growth of Echinostoma malayanum at high worm densities. Mohandas and Nadakal (1978) have shown retarded growth of Echinostoma malayanum at high worm densities.…”

“…Echinostoma malayanum causes mucosal destruction, edema of the lamina propria and hyperplasia of the epithelial cells in experimental rats (Mohandas and Nadakal, 1978). The backwardly-pointed collar spines most likely help the worm to secure itself in the mucosa.…”

“…Some information is available on intraspecific crowding with intestinal trematodes. Other reports on crowding with intestinal trematodes include those by Willey (1941), Fried and Nelson (1978), Mohandas and Nadakal (1978), Fried and Freebome (1984), and Yao et al (1991). Other reports on crowding with intestinal trematodes include those by Willey (1941), Fried and Nelson (1978), Mohandas and Nadakal (1978), Fried and Freebome (1984), and Yao et al (1991).…”

Interspecific interactions in trematode communities.

“…Trematodes mature and mate with their hermaphroditic conspecifics (although schistomes have separate sexes) and pass eggs (often with the host's feces) out of the host. If resources become limited in the host due to competition with other parasites, growth and egg production can suffer as can be seen in experimentally induced, highintensity infections with echinostomes (Mohandas and Nadakal, 1978).…”