Is anthelmintic resistance a concern for heartworm control? What can we learn from the human filariasis control programs?
Identifieur interne : 007F72 ( Main/Curation ); précédent : 007F71; suivant : 007F73Is anthelmintic resistance a concern for heartworm control? What can we learn from the human filariasis control programs?
Auteurs : R K Prichard [Canada]Source :
- Veterinary parasitology [ 0304-4017 ] ; 2005.
Descripteurs français
- KwdFr :
- Animaux, Antihelminthiques (pharmacologie), Canaux chlorure (), Dirofilaria immitis (), Dirofilaria immitis (croissance et développement), Dirofilariose (), Dirofilariose (traitement médicamenteux), Filaricides (pharmacologie), Filariose lymphatique (), Humains, Macrolides (pharmacologie), Onchocercose (), Résistance aux substances (génétique), Spécificité d'espèce, Tests de sensibilité parasitaire.
- MESH :
- croissance et développement : Dirofilaria immitis.
- génétique : Résistance aux substances.
- pharmacologie : Antihelminthiques, Filaricides, Macrolides.
- traitement médicamenteux : Dirofilariose.
- Animaux, Canaux chlorure, Dirofilaria immitis, Dirofilariose, Filariose lymphatique, Humains, Onchocercose, Spécificité d'espèce, Tests de sensibilité parasitaire.
English descriptors
- KwdEn :
- Animals, Anthelmintics (pharmacology), Chloride Channels (drug effects), Dirofilaria immitis (drug effects), Dirofilaria immitis (growth & development), Dirofilariasis (drug therapy), Dirofilariasis (prevention & control), Drug Resistance (genetics), Elephantiasis, Filarial (prevention & control), Filaricides (pharmacology), Humans, Macrolides (pharmacology), Onchocerciasis (prevention & control), Parasitic Sensitivity Tests, Species Specificity.
- MESH :
- chemical , drug effects : Chloride Channels.
- chemical , pharmacology : Anthelmintics, Filaricides, Macrolides.
- drug effects : Dirofilaria immitis.
- drug therapy : Dirofilariasis.
- genetics : Drug Resistance.
- growth & development : Dirofilaria immitis.
- prevention & control : Dirofilariasis, Elephantiasis, Filarial, Onchocerciasis.
- Animals, Humans, Parasitic Sensitivity Tests, Species Specificity.
Abstract
Heartworm prophylaxis is currently largely dependent on the ability of avermectins and milbemycins to arrest the development of third and fourth stages of Dirofilaria immitis for prolonged periods, without producing adulticidal effects. Major control programs, dependent on the activity of ivermectin, are being implemented for human onchocerciasis and lymphatic filariasis. The avermectins and milbemycins act on glutamate-gated and gamma-aminobutyrate-gated chloride channel subunit proteins in nematodes. Ivermectin resistance has been widely described in trichostrongylid nematodes of ruminants. There is evidence that when ivermectin resistance occurs in nematodes, there may be selection on some, but not all of the genes that code for ligand-gated chloride channel subunit proteins as well as on some ABC-transporter genes, whose products may be involved in regulating macrocyclic lactone drug concentrations at receptors, and on some structural protein genes of amphidial neurones. Although ivermectin resistance has not been reported in filarial nematodes, there have recently been reports of suboptimal responses to ivermectin in Onchocerca volvulus. Evidence has been found of ivermectin selection on at least ABC-transporter genes and some neuronal structural protein genes in O. volvulus. To date, there is no evidence of avermectin/milbemycin resistance in D. immitis, also a filarial nematode. Chemotherapy against trichostrongylids of animals, human filariae, and D. immitis, relies on avermectins or milbemycins. However, control involves targeting different stages or processes in the nematode life cycles, different control strategies, different proportions of the nematode population in refugia, and different drug dosage rates. Consideration of the proportion of the D. immitis population normally in refugia, the life cycle stage targeted, and the anthelmintic dosages used suggest that it is unlikely that significant avermectin/milbemycin resistance will be selected in D. immitis with current treatment strategies.
DOI: 10.1016/j.vetpar.2005.04.008
PubMed: 16198824
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<term>Dirofilaria immitis (drug effects)</term>
<term>Dirofilaria immitis (growth & development)</term>
<term>Dirofilariasis (drug therapy)</term>
<term>Dirofilariasis (prevention & control)</term>
<term>Drug Resistance (genetics)</term>
<term>Elephantiasis, Filarial (prevention & control)</term>
<term>Filaricides (pharmacology)</term>
<term>Humans</term>
<term>Macrolides (pharmacology)</term>
<term>Onchocerciasis (prevention & control)</term>
<term>Parasitic Sensitivity Tests</term>
<term>Species Specificity</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Antihelminthiques (pharmacologie)</term>
<term>Canaux chlorure ()</term>
<term>Dirofilaria immitis ()</term>
<term>Dirofilaria immitis (croissance et développement)</term>
<term>Dirofilariose ()</term>
<term>Dirofilariose (traitement médicamenteux)</term>
<term>Filaricides (pharmacologie)</term>
<term>Filariose lymphatique ()</term>
<term>Humains</term>
<term>Macrolides (pharmacologie)</term>
<term>Onchocercose ()</term>
<term>Résistance aux substances (génétique)</term>
<term>Spécificité d'espèce</term>
<term>Tests de sensibilité parasitaire</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anthelmintics</term>
<term>Filaricides</term>
<term>Macrolides</term>
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<keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Dirofilaria immitis</term>
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<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antihelminthiques</term>
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<term>Macrolides</term>
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<keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Dirofilariasis</term>
<term>Elephantiasis, Filarial</term>
<term>Onchocerciasis</term>
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<term>Canaux chlorure</term>
<term>Dirofilaria immitis</term>
<term>Dirofilariose</term>
<term>Filariose lymphatique</term>
<term>Humains</term>
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<front><div type="abstract" xml:lang="en">Heartworm prophylaxis is currently largely dependent on the ability of avermectins and milbemycins to arrest the development of third and fourth stages of Dirofilaria immitis for prolonged periods, without producing adulticidal effects. Major control programs, dependent on the activity of ivermectin, are being implemented for human onchocerciasis and lymphatic filariasis. The avermectins and milbemycins act on glutamate-gated and gamma-aminobutyrate-gated chloride channel subunit proteins in nematodes. Ivermectin resistance has been widely described in trichostrongylid nematodes of ruminants. There is evidence that when ivermectin resistance occurs in nematodes, there may be selection on some, but not all of the genes that code for ligand-gated chloride channel subunit proteins as well as on some ABC-transporter genes, whose products may be involved in regulating macrocyclic lactone drug concentrations at receptors, and on some structural protein genes of amphidial neurones. Although ivermectin resistance has not been reported in filarial nematodes, there have recently been reports of suboptimal responses to ivermectin in Onchocerca volvulus. Evidence has been found of ivermectin selection on at least ABC-transporter genes and some neuronal structural protein genes in O. volvulus. To date, there is no evidence of avermectin/milbemycin resistance in D. immitis, also a filarial nematode. Chemotherapy against trichostrongylids of animals, human filariae, and D. immitis, relies on avermectins or milbemycins. However, control involves targeting different stages or processes in the nematode life cycles, different control strategies, different proportions of the nematode population in refugia, and different drug dosage rates. Consideration of the proportion of the D. immitis population normally in refugia, the life cycle stage targeted, and the anthelmintic dosages used suggest that it is unlikely that significant avermectin/milbemycin resistance will be selected in D. immitis with current treatment strategies.</div>
</front>
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