Background Lymphocytic‐plasmacytic enteritis is the common form of idiopathic inflammatory bowel disease (IBD) in dogs. In human IBD, disturbances of amino acid metabolism have been demonstrated to be involved in the pathophysiology of IBD. Therefore, plasma amino acid profile might represent a novel marker of human IBD. Objectives To determine the plasma amino acid profiles of dogs with IBD and its usefulness as a novel marker of IBD in dogs. Animals Fasting blood plasma was obtained from 10 dogs with IBD and 12 healthy dogs. Methods All IBD dogs were prospectively included in this study, and heparinized blood samples were collected. The plasma concentrations of 21 amino acids were determined using the ninhydrin method. The relationships among the plasma amino acid concentrations and plasma C‐reactive protein (CRP) concentration, canine chronic enteropathy clinical activity index (CCECAI), and overall World Small Animal Veterinary Association (WSAVA) score were investigated. Results Median concentration (nmol/mL) of methionine [46.2; range, 30.0‐59.3], proline [119.4; range, 76.7‐189.2], serine [115.1; range, 61.4‐155.9], and tryptophan [17.4; range, 11.9‐56.3]) were significantly lower than in control dogs [62.6; range, 51.0‐83.6, 199.1; range, 132.5‐376.7, 164.3; range, 124.7‐222.9, and 68.3; range, 35.7‐94.8, respectively]. A negative correlation was identified between the plasma serine concentration and CCECAI (r _s = −.67, P = .03), but there were no correlations between plasma amino acid concentrations and CRP concentration or overall WSAVA score. Conclusions and Clinical Importance Plasma serine concentration might represent a novel maker of IBD in dogs.

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The stability of the characteristics of the diminazene aceturate (DA)-resistant B. gibsoni isolate was initially determined invitro. Part of the DA-resistant B. gibsoni isolate was cultured without DA for 4 weeks, and then newly exposed to 200 ng/ml DA. As a result, this isolate could proliferate the same as the DA-resistant isolate, indicating that the characteristic of DA resistance was stable in the DA-resistant isolate. Additionally, the level of parasitemia in the DA-resistant isolate was comparatively lower than in the wild-type, suggesting that the proliferation potential of the DA-resistant isolate would be lower than that of the wild-type. Subsequently, to investigate the involvement of mitochondrial DNA (mtDNA) in DA resistance in B. gibsoni, the nucleotide sequences and deduced amino acid sequences of mitochondrial genes such as COXI, COXIII, and CYTb genes of the DA-resistant isolate, were compared with those of the wild-type. As a result, these three genes were not altered in the DA-resistant B. gibsoni isolate. Moreover, the transcription levels of COXI, COXIII, and CYTb genes were observed by semi-quantitative RT-PCR. As a result, the gene transcription of those genes in the DA-resistant isolate was not significantly altered. These results indicated that DA did not affect mtDNA directly in DA-resistant B. gibsoni. Thus, it is suggested that mtDNA should not be deeply involved in DA resistance in B. gibsoni.