Retrospective Evaluation of the Effect of Heart Rate on Survival in Dogs with Atrial Fibrillation

Background

Atrial fibrillation (AF) usually is associated with a rapid ventricular rate. The optimal heart rate (HR) during AF is unknown.

Hypothesis/Objectives

Heart rate affects survival in dogs with chronic AF.

Animals

Forty‐six dogs with AF and 24‐hour ambulatory recordings were evaluated.

Methods

Retrospective study. Holter‐derived HR variables were analyzed as follows: mean HR (meanHR, 24‐hour average), minimum HR (minHR, 1‐minute average), maximum HR (maxHR, 1‐minute average). Survival times were recorded from the time of presumed adequate rate control. The primary endpoint was all‐cause mortality. Cox proportional hazards analysis identified variables independently associated with survival; Kaplan‐Meier survival analysis estimated the median survival time of dogs with meanHR <125 bpm versus ≥125 bpm.

Results

All 46 dogs had structural heart disease; 31 of 46 had congestive heart failure (CHF), 44 of 46 received antiarrhythmic drugs. Of 15 dogs with cardiac death, 14 had CHF. Median time to all‐cause death was 524 days (Interquartile range (IQR), 76–1,037 days). MeanHR was 125 bpm (range, 62–203 bpm), minHR was 82 bpm (range, 37–163 bpm), maxHR was 217 bpm (range, 126–307 bpm). These were significantly correlated with all‐cause and cardiac‐related mortality. For every 10 bpm increase in meanHR, the risk of all‐cause mortality increased by 35% (hazard ratio, 1.35; 95% CI, 1.17–1.55; P < 0.001). Median survival time of dogs with meanHR<125 bpm (n = 23) was significantly longer (1,037 days; range, 524‐open) than meanHR ≥125 bpm (n = 23; 105 days; range, 67–267 days; P = 0.0012). Mean HR was independently associated with all‐cause and cardiovascular mortality (P < 0.003).

Conclusions and Clinical Importance

Holter‐derived meanHR affects survival in dogs with AF. Dogs with meanHR <125 bpm lived longer than those with meanHR ≥ 125 bpm.     

Genetic characterisation of protective vaccine responses in sheep using multi-valent Dichelobacter nodosus vaccines

Protective vaccine responses to nine distinct serogroups of Dichelobacter nodosus (serogroups A-I) can be readily measured by serogroup-specific K-agglutinating antibody titres. On the basis of a large quantitative genetic experiment (1200 progeny from 129 sire groups), it was shown that variation in antibody responses following vaccination with a multi-valent pilus antigen D. nodosus vaccine (serogroups A-I) is, in part, under genetic control and thus heritable. Based on the genetic relationships between antibody responses to all nine antigens, results suggested that both genes for a broad-based and genes for serogroup-specific response contributed to genetic variation in vaccine response. Furthermore, preliminary data in 389 progeny showed that polymorphism within the ovine major histocompatibility (MHC) based on serological classification accounted for a significant proportion of the variation in vaccine responses. In subsequent experimentation, we examined the importance of genetic polymorphism within the ovine MHC, and the possibility of genes outside the MHC for their involvement in antigen-specific and broad-based vaccine response. Within two large half sib families(131, and 143 progeny), four MHC haplotypes were investigated and found to be associated with differential antibody responses to six out of eight distinct vaccine-antigens presented to the host in a multi-valent vaccine. The model used here shows how well characterised immunogens, quantitative genetic experimentation, and molecular gene mapping tools can be used to unravel genetic differences in host responses to commercial vaccines.     

Diagnostic features, confirmation and disease progression in 28 cases of lethal acrodermatitis of bull terriers

Lethal acrodermatitis (LAD) is a genetically determined metabolic disease of bull terriers first described in the USA in the 1980s. In this study, the largest so far reported, 28 bull terriers born in the UK were diagnosed as suffering from LAD, and the clinical findings and the progression of the disease with time are described. The main characteristics of LAD are stunting, splayed digits, eating difficulties, skin disease of the face and feet, and increased susceptibility to microbial infections. In older dogs, paronychia, nail disease and hyperkeratosis of the footpads develops, becoming severe in dogs over six months of age. A diagnosis of LAD can be strongly suspected in any bull terrier showing a combination of the aforementioned signs from an early age. Dermatohistopathological demonstration of marked parakeratotic hyperkeratosis is strongly supportive of the diagnosis of LAD and, in association with the typical clinical findings, is sufficient to confirm a diagnosis. Although many of the clinical signs and the pathology of this condition suggest zinc deficiency, the measurement of blood zinc levels as a diagnostic aid is of limited value.     

Malassezia and Candida infections in bull terriers with lethal acrodermatitis

In 12 cases of lethal acrodermatitis (LAD), four sampling techniques (brush, swab, scrape and adhesive tape strip) were used to study the distribution of yeasts in various body sites and these results were compared with those from five cases of atopic dermatitis and those of 10 normal dogs. Malassezia was frequently isolated from lesional and non-lesional skin and haircoat, footpads, nails and mucous membranes from dogs with either LAD or atopic dermatitis, although, generally, more Malassezia organisms were isolated from LAD cases. In normal dogs, Malassezia was most frequently recovered from the ear canal and the perianal skin. Candida was isolated frequently from dogs with LAD, but only a single isolate of this yeast was found in the other two groups. Fungal hyphae and pseudohyphae, probably Candida albicans, could be detected in samples collected from the nails and footpads of dogs with LAD. Both Malassezia and Candida could be isolated using all four sampling techniques. The MacKenzie (toothbrush) technique and adhesive tape strip cultures proved simple methods for the semiquantitative evaluation of yeasts. The high recovery rate of Malassezia and Candida from dogs with LAD is probably related to immune dysfunction, particularly T-cell dysfunction, known to be present in these dogs. C albicans infection may in part be responsible for the pathogenic changes of the nails and footpads commonly seen in cases of LAD.     

A directed search in the region of GDF8 for quantitative trait loci affecting carcass traits in Texel sheep

A directed search for QTL affecting carcass traits was carried out in the region of growth differentiation factor 8 (GDF8, also known as myostatin) on ovine chromosome 2 in seven Texel-sired half-sib families totaling 927 progeny. Weights were recorded at birth, weaning, ultrasound scanning, and slaughter. Ultrasonic measures of LM cross-sectional dimensions and s.c. fat above the LM were made, with the same measurements made on the LM after slaughter. Following slaughter, linear measurements of carcass length and width were made on all carcasses, and legs and loins from 540 lambs were dissected. Genotyping was carried out using eight microsatellite markers from FCB128 to RM356 on OAR 2 and analyzed using Haley-Knott regression. There was no evidence for QTL for growth rates or linear carcass traits. There was some evidence for QTL affecting LM dimensions segregating in some sire families, although it was not consistent between ultrasound and carcass measures of the same traits. There was strong and consistent evidence for a QTL affecting muscle and fat traits in the leg that mapped between markers BM81124 and BULGE20 for the four sires that were heterozygous in this region, but not for the three sires that were homozygous. The size of the effect varied across the four sires, ranging from 0.5 to 0.9 of an adjusted SD for weight-adjusted leg muscle traits, and ranging from 0.6 to 1.2 of an adjusted SD for weight-adjusted leg fat traits. The clearest effect shown was for multivariate analysis combining all leg muscle and fat traits analyzed across sires, where the -log(10) probability was 14. Animals carrying the favorable haplotype had 3.3% more muscle and 9.9% less fat in the leg relative to animals carrying other haplotypes. There was evidence for a second peak in the region of marker TEXAN2 for one sire group. It seems that a QTL affecting muscle and fat traits exists within the New Zealand Texel population, and it maps to the region of GDF8 on OAR2.     

EXPERIMENTAL POISONING OF HORSES AND CATTLE WITH SWAINSONA CANESCENS VAR HORNIANA

Horses and cattle fed swainsona ( Swainsona canescens var horniana ) over a period of 8 to 10 weeks lost condition and became incoordinated and hypersensitive. Histotogical examination of tissues from affected animals revealed the characteristic changes of widespread cellular vacuolation and axonal spheroids in the CNS.
Cattle withdrawn from the toxic plant after being fed for varying periods up to 8 weeks returned to normal.
Serum α-mannosidase activity declined significantly in cattle during the test period, whereas in horses the activity rose. Serum alkaline phosphatase levels increased significantly in cattle but not in horses.
The similarity of the clinical signs of disease in horses was noted to those seen in Indigofera linnaei poisoning (Birdsville disease). Differential diagnosis can be made by botanical observations and by an increased frequency of vacuolated lymphocytes in the blood in swainsona poisoning.