Objective—To determine the prevalence and clinical
implications of anthelmintic resistance in cyathostomes
Animals—80 horses on 10 farms in a 5-county region
of northeast Georgia.
Procedure—On each farm, horses were stratified in
descending order according to pretreatment fecal egg
count (FEC), blocked into groups of 4, and then randomly
assigned to 1 of 4 treatment groups: no treatment
(controls), and treatment with pyrantel
pamoate, fenbendazole, or ivermectin. Fecal samples
were collected 24 hours prior to treatment and 2, 4,
and 6 weeks after treatment for determination of
FEC. Mean percentage of reduction in FEC was then
calculated for each treatment group. For horses from
each farm, the efficacy of each anthelmintic was categorized
on the basis of mean percentage of reduction
in FEC at 2 weeks after treatment (< 80% reduction
= ineffective; 80 to 90% reduction = equivocal;
and > 90% reduction = effective).
Results—Pyrantel pamoate was effective at reducing
FEC in horses from 7 farms, ineffective in horses from
2 farms, and equivocal in horses from 1 farm.
Fenbendazole was ineffective at reducing FEC in horses
from 9 farms and equivocal in horses from 1 farm.
Ivermectin was effective at reducing FEC in horses
from all 10 farms.
Conclusions and Clinical Relevance—Results suggest
that cyathostome resistance to fenbendazole is
highly prevalent, and resistance to pyrantel pamoate
is high enough to warrant concern. Resistance to ivermectin
was not detected. On the basis of these data,
it appears that ivermectin continues to be fully effective
in horses. However, too few farms were used in
this study to determine the prevalence of cyathostome
resistance to ivermectin. Therefore, the efficacy
of ivermectin should continue to be monitored closely.
(J Am Vet Med Assoc 2001;218:1957–1960)
To characterize transcription of profibrotic mediators in renal tissues of cats with ischemia-induced chronic kidney disease (CKD).
Banked renal tissues from 6 cats with experimentally induced CKD (RI group) and 8 healthy control cats.
For cats of the RI group, both kidneys were harvested 6 months after ischemia was induced for 90 minutes in 1 kidney. For control cats, the right kidney was evaluated. All kidney specimens were histologically examined for fibrosis, inflammation, and tubular atrophy. Renal tissue homogenates underwent reverse transcription quantitative PCR assay evaluation to characterize gene transcription of hypoxia-inducible factor-1α (HIF-1α), matrix metalloproteinase (MMP)-2, MMP-7, MMP-9, tissue inhibitor of metalloproteinase-1 (TIMP-1), transforming growth factor-β1, and vascular endothelial growth factor A. Gene transcription and histologic lesions were compared among ischemic and contralateral kidneys of the RI group and control kidneys.
Ischemic kidneys had greater transcript levels of MMP-7, MMP-9, and transforming growth factor-β1 relative to control kidneys and of MMP-2 relative to contralateral kidneys. Transcription of TIMP-1 was upregulated and that of vascular endothelial growth factor A was downregulated in ischemic and contralateral kidneys relative to control kidneys. Transcription of HIF-1α did not differ among kidney groups. For ischemic kidneys, there were strong positive correlations between transcription of HIF-1α, MMP-2, MMP-7, and TIMP-1 and severity of fibrosis.
CONCLUSIONS AND CLINICAL RELEVANCE
Transcription of genes involved in profibrotic pathways remained altered in both kidneys 6 months after transient renal ischemia. This suggested that a single unilateral renal insult can have lasting effects on both kidneys.
To use RNA sequencing (RNAseq) to characterize renal transcriptional activities of genes associated with proinflammatory and profibrotic pathways in ischemia-induced chronic kidney disease (CKD) in cats.
Banked renal tissues from 6 cats with experimentally induced CKD (renal ischemia [RI] group) and 9 healthy cats (control group).
Transcriptome analysis with RNAseq, followed by gene ontology and cluster analyses, were performed on banked tissue samples of the right kidneys (control kidneys) from cats in the control group and of both kidneys from cats in the RI group, in which unilateral (right) RI had been induced 6 months before the cats were euthanized and the ischemic kidneys (IKs) and contralateral nonischemic kidneys (CNIKs) were harvested. Results for the IKs, CNIKs, and control kidneys were compared to identify potential differentially expressed genes and overrepresented proinflammatory and profibrotic pathways.
Genes from the gene ontology pathways of collagen binding (eg, transforming growth factor-β1), metalloendopeptidase activity (eg, metalloproteinase [MMP]-7, MMP-9, MMP-11, MMP-13, MMP-16, MMP-23B, and MMP-28), chemokine activity, and T-cell migration were overrepresented as upregulated in tissue samples of the IKs versus control kidneys. Genes associated with the extracellular matrix (eg, TIMP-1, fibulin-1, secreted phosphoprotein-1, matrix Gla protein, and connective tissue growth factor) were upregulated in tissue samples from both the IKs and CNIKs, compared with tissues from the control kidneys.
CONCLUSIONS AND CLINICAL RELEVANCE
Unilateral ischemic injury differentially altered gene expression in both kidneys, compared with control kidneys. Fibulin-1, secreted phosphoprotein-1, and matrix Gla protein may be candidate biomarkers of active kidney injury in cats.