Echinostoma revolutum: Resistance to secondary and superimposed infections in mice
A complete or almost complete resistance (94–100%) to a superimposed Echinostoma revolutum infection existed in mice harboring 20-, 30-, and 40-day-old infections in the range of 2–4 to 30–35 worms, but no resistance was found at challenge Day 10. A similar high level of resistance (85–100%) also ex...
Gespeichert in:
Veröffentlicht in: | Experimental parasitology 1986-06, Vol.61 (3), p.311-318 |
---|---|
Hauptverfasser: | , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | A complete or almost complete resistance (94–100%) to a superimposed
Echinostoma revolutum infection existed in mice harboring 20-, 30-, and 40-day-old infections in the range of 2–4 to 30–35 worms, but no resistance was found at challenge Day 10. A similar high level of resistance (85–100%) also existed in mice for at least 6 weeks after natural expulsion of a primary 6 metacercarial infection and for at least 5 weeks after anthelmintic termination of a 30-day-old 20 metacercarial infection. Thymus-deficient nude mice failed to develop resistance to a superimposed infection, and the resistance in normal mice was inhibited by corticosteroid treatment. These findings are all in favor of a host immune response being responsible for the resistance against both a secondary and a superimposed infection. Nearly all the worms of a superimposed infection were, in resistant mice, expelled prior to 24 hr following infection (rapid expulsion), and the few worms circumventing this early expulsion persisted for at least 8 days. Newly excysted juvenile worms implanted intraduodenally into resistant mice were rejected to the same degree as juvenile worms from an oral metacercarial infection indicating that the newly excysted juvenile worms are the target of the host immune response. However, 7-day-old worms implanted intraduodenally into resistant mice survived indicating that adaptation to the host immune response had occurred. In conclusion, this host-parasite model is an example of concomitant immunity because the immunological mechanism responsible for the expulsion of the superimposed infection had no effect on the number of primary worms present. |
---|---|
ISSN: | 0014-4894 1090-2449 |
DOI: | 10.1016/0014-4894(86)90186-4 |