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Induction of protective immunity to Brugia pahangi in jirds by drug-abbreviated infection

Published online by Cambridge University Press:  05 June 2009

Y. Horii
Affiliation:
Department of Medical Zoology, Nagasaki University School of Medicine, Sakamoto-machi, Nagasaki 852, Japan
H. Nakanishi
Affiliation:
Department of Medical Zoology, Nagasaki University School of Medicine, Sakamoto-machi, Nagasaki 852, Japan
A. Mori
Affiliation:
Department of Medical Zoology, Nagasaki University School of Medicine, Sakamoto-machi, Nagasaki 852, Japan
M. Ueda
Affiliation:
Department of Medical Zoology, Nagasaki University School of Medicine, Sakamoto-machi, Nagasaki 852, Japan
K. Kurokawa
Affiliation:
Department of Medical Zoology, Nagasaki University School of Medicine, Sakamoto-machi, Nagasaki 852, Japan
M. Zaitsu
Affiliation:
Department of Medical Zoology, Nagasaki University School of Medicine, Sakamoto-machi, Nagasaki 852, Japan
T. Oda
Affiliation:
Department of General Education, School of Allied Medical Sciences, Nagasaki University, Sakamoto-machi, Nagasaki 852, Japan
K. Fujita
Affiliation:
Department of Medical Zoology, Tokyo Medical and Dental University, Yushima, Bunkyo-ku 113, Japan

Abstract

Protective immunity of homologous challenge infection was examined in jirds after drug-abbreviated infection with Brugia pahangi. Mebendazole (MBZ) treatment at the early prepatent (5–7 weeks of post infection) or the late prepatent (7–9 weeks of post infection) period was highly effective in causing almost complete eradication of the primary infection. After challenge infection, the worm burden was significantly reduced 19% (31·1 in average) and 77% (9·5) to that of the controls (38·8 and 41·7), respectively. The magnitude of eosinophil response paralleled the degree of protection. No or only a few microfilariae were seen after challenge infection in jirds treated during the prepatent periods. They were also resistant to intravenous challenge with the microfilariae of B. pahangi. MBZ treatment at the patent period was, on the contrary, incomplete against primarily infected adult worms, and was not able to induce either significant protection (30·1 vs 33·1 in control) or eosinophil response to the challenge infection.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1992

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