Brugia pahangi in rats: increasing the number of infective larvae inoculated increases the percentage of microfilaremic rats.
Identifieur interne : 005415 ( PubMed/Checkpoint ); précédent : 005414; suivant : 005416Brugia pahangi in rats: increasing the number of infective larvae inoculated increases the percentage of microfilaremic rats.
Auteurs : R. Lawrence [Royaume-Uni] ; D A DenhamSource :
- The Journal of parasitology [ 0022-3395 ] ; 1991.
Descripteurs français
- KwdFr :
- MESH :
- croissance et développement : Brugia, Microfilaria.
- parasitologie : Filariose lymphatique.
- sang : Filariose lymphatique.
- Animaux, Femelle, Mâle, Rats.
English descriptors
- KwdEn :
- MESH :
- blood : Elephantiasis, Filarial.
- growth & development : Brugia, Microfilariae.
- parasitology : Elephantiasis, Filarial.
- Animals, Female, Male, Rats.
Abstract
One hundred Brugia pahangi infective larvae (L3) caused microfilaremic (mf + ve) infection in 56% of inbred PVG rats. Adult worms were recovered consistently from infected rats but worm recovery was very low, only 1-3% of L3 inoculated survived to adulthood and the worms were dispersed in a wide range of anatomical sites. This suggested that lack of microfilaremia may be due to the low probability of male and female worms meeting in the same site and thus may be numerically and topographically based. When the number of infective larvae inoculated was increased to 500, the percentage of mf + ve infections in rats also increased to 94%, corroborating the hypothesis that lack of mf was not due to an immune response. In a further experiment all infected rats had lost both mf and adult worms by day 420. It has yet to be established whether final rejection of the parasite is due to immunity.
PubMed: 1992091
Affiliations:
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pubmed:1992091Le document en format XML
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<front><div type="abstract" xml:lang="en">One hundred Brugia pahangi infective larvae (L3) caused microfilaremic (mf + ve) infection in 56% of inbred PVG rats. Adult worms were recovered consistently from infected rats but worm recovery was very low, only 1-3% of L3 inoculated survived to adulthood and the worms were dispersed in a wide range of anatomical sites. This suggested that lack of microfilaremia may be due to the low probability of male and female worms meeting in the same site and thus may be numerically and topographically based. When the number of infective larvae inoculated was increased to 500, the percentage of mf + ve infections in rats also increased to 94%, corroborating the hypothesis that lack of mf was not due to an immune response. In a further experiment all infected rats had lost both mf and adult worms by day 420. It has yet to be established whether final rejection of the parasite is due to immunity.</div>
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<Abstract><AbstractText>One hundred Brugia pahangi infective larvae (L3) caused microfilaremic (mf + ve) infection in 56% of inbred PVG rats. Adult worms were recovered consistently from infected rats but worm recovery was very low, only 1-3% of L3 inoculated survived to adulthood and the worms were dispersed in a wide range of anatomical sites. This suggested that lack of microfilaremia may be due to the low probability of male and female worms meeting in the same site and thus may be numerically and topographically based. When the number of infective larvae inoculated was increased to 500, the percentage of mf + ve infections in rats also increased to 94%, corroborating the hypothesis that lack of mf was not due to an immune response. In a further experiment all infected rats had lost both mf and adult worms by day 420. It has yet to be established whether final rejection of the parasite is due to immunity.</AbstractText>
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