The development of resistance to glycarbylamide and 2-chloro-4-nitrobenzamide in Eimeria tenella in chicks

Parasitology ◽  
1966 ◽  
Vol 56 (1) ◽  
pp. 25-37 ◽  
Author(s):  
S. J. Ball
Keyword(s):  
Drug Resistance ◽  
Resistant Strain ◽  
Parent Strain ◽  
Technical Assistance ◽  
Eimeria Tenella ◽  
Single Test ◽  
Normal Parent ◽  
Twofold Increase ◽  
Development Of Resistance ◽  
Resistant Strains

A twofold increase in resistance to glycarbylamide was induced in a strain of Eimeria tenella in chicks. This strain remained susceptible to amprolium, nicarbazin, nitrofurazone, zoalene, 3,5-dinitrobenzamide, 2-chloro-4-nitrobenzamide (M & B 5921) and spiramycin.At least an eightfold resistance to 2-chloro-4-nitrobenzamide (M & B 5921) was developed in another strain of E. tenella. This strain was also resistant to nitrofurazone, zoalene and 3,5-dinitrobenzamide, but not to glycarbylamide, amprolium, nicarbazin and spiramycin.A single test showed no transfer of drug-resistance when the two resistant strains were given simultaneously to the same birds.When a small number of parasites of a glycarbylamide-resistant strain of E. tenella was introduced into a larger inoculum of the normal parent strain, the resistant individuals appeared to diminish in number during passages through untreated chicks.I wish to thank Mrs B. M. Mitchell, Miss C. A. Hitchcock and Miss J. Watkins for technical assistance at various stages of the work.

The development of drug-resistant strains of Eimeria maxima in the laboratory

Parasitology ◽  
1975 ◽  
Vol 71 (1) ◽  
pp. 153-165 ◽  
Author(s):  
C. C. Norton ◽  
L. P. Joyner
Keyword(s):  
Drug Administration ◽  
Resistant Strain ◽  
Parent Strain ◽  
Drug Resistant ◽  
Development Of Resistance ◽  
Eimeria Maxima ◽  
Resistant Strains ◽  
Drug Dependent ◽  
Drug Resistant Strains

The development of strains of Eimeria maxima resistant to buquinolate, methyl benzoquate, clopidol, sulphaquinoxaline and robenidine is described. It was not possible to standardize a schedule of inoculations and drug administration, which would enable the development of resistance to the different drugs to be compared directly. Resistance developed most readily to the quinolones. One robenidine-resistant strain proved to be drug-dependent. Dinitolmide showed unusual effects upon sporogony and three attempts to develop resistance against this activity failed. Chicks previously immunized with the parent strain were completely protected against infection with the drug-resistant strains.

scholarly journals UDP-Glycosyltransferases and Albendazole Metabolism in the Juvenile Stages of Haemonchus contortus

2020 ◽  
Vol 11 ◽  
Author(s):  
Pavlína Kellerová ◽  
Martina Navrátilová ◽  
Linh Thuy Nguyen ◽  
Diana Dimunová ◽  
Lucie Raisová Stuchlíková ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Resistant Strain ◽  
Haemonchus Contortus ◽  
Resistance Mechanism ◽  
Constitutive Expression ◽  
Primary Metabolite ◽  
Resistance Development ◽  
Enhanced Solubility ◽  
Juvenile Stages ◽  
Resistant Strains

The nematode Haemonchus contortus, a gastrointestinal parasite of ruminants, can severely burden livestock production. Although anthelmintics are the mainstay in the treatment of haemonchosis, their efficacy diminishes due to drug-resistance development in H. contortus. An increased anthelmintics inactivation via biotransformation belongs to a significant drug-resistance mechanism in H. contortus. UDP-glycosyltransferases (UGTs) participate in the metabolic inactivation of anthelmintics and other xenobiotic substrates through their conjugation with activated sugar, which drives the elimination of the xenobiotics due to enhanced solubility. The UGTs family, in terms of the biotransformation of commonly used anthelmintics, has been well described in adults as a target stage. In contrast, the free-living juvenile stages of H. contortus have attracted less attention. The expression of UGTs considerably varies throughout the life cycle of the juvenile nematodes, suggesting their different roles. Furthermore, the constitutive expression in a susceptible strain with two resistant strains shows several resistance-related changes in UGTs expression, and the exposure of juvenile stages of H. contortus to albendazole (ABZ) and ABZ-sulfoxide (ABZSO; in sublethal concentrations) leads to the increased expression of several UGTs. The anthelmintic drug ABZ and its primary metabolite ABZSO biotransformation, tested in the juvenile stages, shows significant differences between susceptible and resistant strain. Moreover, higher amounts of glycosidated metabolites of ABZ are formed in the resistant strain. Our results show similarly, as in adults, the UGTs and glycosidations significant for resistance-related differences in ABZ biotransformation and warrant further investigation in their individual functions.

scholarly journals A Redox Basis for Metronidazole Resistance in Helicobacter pylori

2009 ◽  
Vol 53 (5) ◽  
pp. 1884-1891 ◽  
Author(s):  
N. O. Kaakoush ◽  
C. Asencio ◽  
F. Mégraud ◽  
G. L. Mendz
Keyword(s):  
Helicobacter Pylori ◽  
Resistant Strain ◽  
Gene Mutations ◽  
Thioredoxin Reductase ◽  
Matched Pair ◽  
Specific Gene ◽  
Two Dimensional Gel Electrophoresis ◽  
Development Of Resistance ◽  
Metronidazole Resistance ◽  
Resistant Strains

ABSTRACT Metronidazole resistance in Helicobacter pylori has been attributed to mutations in rdxA or frxA. Insufficient data correlating RdxA and/or FrxA with the resistant phenotype, and the emergence of resistant strains with no mutations in either rdxA or frxA, indicated that the molecular basis of H. pylori resistance to metronidazole required further characterization. The rdxA and frxA genes of four matched pairs of metronidazole-susceptible and -resistant strains were sequenced. The resistant strains had mutations in either rdxA, frxA, neither gene, or both genes. The reduction rates of five substrates suggested that metabolic differences between susceptible and resistant strains cannot be explained only by mutations in rdxA and/or frxA. A more global approach to understanding the resistance phenotype was taken by employing two-dimensional gel electrophoresis combined with tandem mass spectrometry analyses to identify proteins differentially expressed by the matched pair of strains with no mutations in rdxA or frxA. Proteins involved in the oxireduction of ferredoxin were downregulated in the resistant strain. Other redox enzymes, such as thioredoxin reductase, alkyl hydroperoxide reductase, and superoxide dismutase, showed a pI change in the resistant strain. The data suggested that metronidazole resistance involved more complex metabolic changes than specific gene mutations, and they provided evidence of a role for the intracellular redox potential in the development of resistance.

Eimeria tenella in chickens: development of resistance to quinolone anticoccidial drugs

Parasitology ◽  
1975 ◽  
Vol 71 (1) ◽  
pp. 41-49 ◽  
Author(s):  
H. D. Chapman
Keyword(s):  
Drug Resistance ◽  
Weight Gain ◽  
Liquid Nitrogen ◽  
Selection Pressure ◽  
Drug Tolerance ◽  
Eimeria Tenella ◽  
Cross Resistance ◽  
Drug Selection ◽  
Laboratory Conditions ◽  
Development Of Resistance

The development of drug resistance by the present Houghton strain of Eimeria tenella to the quinolones, methyl benzoquate and buquinolate, was found to take place after a single experimental passage. The development of resistance was independent of drug selection pressure and showed cross resistance to other quinolones, but not to amprolium and robenidine. When the Weybridge, Beltsville and Elberfeld strains of E. tenella were compared under similar laboratory conditions, the Weybridge and Elberfeld strains developed resistance to methyl benzoquate after 6 passages and the Beltsville after 5. Studies on the response of the Houghton strain to methyl benzoquate and buquinolate revealed that the drugs did not completely control the infection as measured by weight gain and that oocyst production was not suppressed. These observations indicate that the strain had already acquired some resistance to these drugs. This was confirmed by examining the resistance to methyl benzoquate of a culture of the Houghton strain of E. tenella which had been stored frozen in liquid nitrogen since 1969. This showed full sensitivity to the drug and developed resistance after 8 passages. This suggests that drug tolerance has been acquired by the Houghton strain since 1969.Oocyst lines were established from the Houghton strain by infecting single birds with approximately 10 oocysts. Eleven of these lines were found to be sensitive to methyl benzoquate, and nine to give rise to resistant parasites. It is concluded that the Houghton strain is contaminated by a small number of resistant oocysts which can be eliminated from a culture by dilution of the challenge inoculum. One of these Houghton oocyst lines, sensitive to methyl benzoquate, developed resistance after 8 serial passages.

Selection of a BHC-resistant Strain of Drosophila melanogaster Mg

1953 ◽  
Vol 44 (2) ◽  
pp. 395-400 ◽  
Author(s):  
F. J. Oppenoorth ◽  
D. Dresden
Keyword(s):  
Drosophila Melanogaster ◽  
Resistant Strain ◽  
Parent Strain ◽  
Laboratory Strain ◽  
Contact Method ◽  
Resistant Parent ◽  
Reciprocal Crosses ◽  
Wild Strains ◽  
Resistant Strains ◽  
Selection Of

Two wild strains of Drosophila and one laboratory strain were selected for resistance to γBHC by a contact method. From each of these three strains equally resistant strains developed in about the same time. They did not become more resistant after prolonged selection. The resistance obtained was further investigated in one of the strains.There was no evidence of any specificity: the susceptibility of the resistant insects to DDT and “Thanite” also appeared to be less than that of the original strains.Although the strains were selected by a contact method they also showed decreased susceptiblity when the poison was applied to the skin and when it was injected. From the reciprocal crosses F1's were obtained the susceptibilities of which were practically the same and differed little from that of the resistant parent strain. It follows that resistance does not depend on cytoplasmatic heredity and that it is incompletely dominant.

scholarly journals Mutations of the Helicobacter pyloriGenes rdxA and pbp1 Cause Resistance against Metronidazole and Amoxicillin

2001 ◽  
Vol 45 (3) ◽  
pp. 962-965 ◽  
Author(s):  
Ralf Paul ◽  
Stefan Postius ◽  
Klaus Melchers ◽  
Klaus P. Schäfer
Keyword(s):  
Helicobacter Pylori ◽  
Resistance Genes ◽  
Resistant Strain ◽  
Parent Strain ◽  
Metronidazole Resistance ◽  
Pcr Products ◽  
Resistant Strains ◽  
H Pylori

ABSTRACT To investigate amoxicillin and metronidazole resistance ofHelicobacter pylori, we compared putative resistance genes between resistant strains obtained in vitro and their sensitive parent strain. All metronidazole-resistant strains hadrdxA mutations, and an amoxicillin-resistant strain hadpbp1 and pbp2 mutations. By transforming PCR products of these mutated genes into antibiotic-sensitive strains, we showed that rdxA null mutations were sufficient for metronidazole resistance, while pbp1mutations contributed to amoxicillin resistance of H. pylori.

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