Adam Gow

Hypovitaminosis D in dogs with inflammatory bowel disease and hypoalbuminaemia.

OBJECTIVES To compare serum vitamin D metabolites and plasma parathyroid hormone concentrations in dogs with inflammatory bowel disease and normal albumin concentration, dogs with inflammatory bowel disease and hypoalbuminaemia, healthy dogs and hospitalised ill dogs with non-gastrointestinal illness. METHODS Serum 25 hydroxyvitamin D and 1,25 dihydroxyvitamin D concentrations were measured in 36 healthy dogs, 49 hospitalised ill dogs with non-gastrointestinal illnesses, 21 dogs with inflammatory bowel disease and normoalbuminaemia and 12 dogs with inflammatory bowel disease and hypoalbuminaemia. Plasma parathyroid hormone and ionised calcium concentrations were measured in a subset of these dogs. RESULTS Concentrations of serum 25 hydroxyvitamin D were lower in hypoalbuminaemic dogs with inflammatory bowel disease than in the healthy dogs (P<0·001), hospitalised ill dogs (P<0·001) and normoalbuminaemic dogs with inflammatory bowel disease (P<0·001). Dogs with inflammatory bowel disease and hypoalbuminaemia had a higher plasma concentration of parathyroid hormone (P<0·01) and lower plasma concentration of ionised calcium (P<0·001) than hospitalised ill dogs. Dogs with inflammatory bowel disease had a positive correlation between serum 25 hydroxyvitamin D concentrations and serum albumin (P<0·0001), serum calcium (P<0·0001) and plasma ionised calcium (P<0·0005) concentrations. CLINICAL SIGNIFICANCE Dogs with inflammatory bowel disease and hypoalbuminaemia frequently have ionised hypocalcaemia, high parathyroid hormone and low serum 25 hydroxyvitamin D concentrations. Further studies are indicated to establish the pathogenesis of this disease complication as well as therapeutic strategies to reverse this state.

Dogs with congenital porto-systemic shunting (cPSS) and hepatic encephalopathy have higher serum concentrations of C-reactive protein than asymptomatic dogs with cPSS

Hepatic encephalopathy (HE) is a cause of significant morbidity and mortality in patients with liver disorders and a wide range of rodent models of HE have been described to facilitate studies into the pathogenesis and treatment of HE. However, it is widely acknowledged that no individual model perfectly mimics human HE and there is a particular need for spontaneous, larger animal models. One common congenital abnormality in dogs is the portosystemic shunt (cPSS) which causes clinical signs that are similar to human HE such as ataxia, disorientation, lethargy and occasionally coma. As inflammation has recently been shown to be associated with HE in humans, we hypothesised that inflammation would similarly be associated with HE in dogs with cPSS. To examine this hypothesis we measured C-reactive protein (CRP) in 30 healthy dogs, 19 dogs with a cPSS and no HE and 27 dogs with a cPSS and overt HE. There was a significant difference in CRP concentration between healthy dogs and dogs with HE (p < 0.001) and between dogs with HE and without HE (p < 0.05). The novel finding that there is an association between inflammation and canine HE strengthens the concept that HE in dogs with cPSS shares a similar pathogenesis to humans with HE. Consequently, dogs with a cPSS may be a good spontaneous model of human HE in which to further examine the role of inflammation and development of HE.

Prevalence of Potentially Pathogenic Enteric Organisms in Clinically Healthy Kittens in the UK

Faecal samples were collected from 57 clinically healthy kittens presented for initial vaccination, in the UK. Routine bacteriological examination identified Salmonella species in one and Campylobacter species in five samples. Polymerase chain reaction (PCR) detected the presence of Campylobacter species in a further four samples. Routine parasitological examination revealed Toxocara species ova in nine (including four kittens stated to have been administered an anthelmintic) and Isospora species in four samples. No Giardia or Cryptosporidium species were detected by routine methods. A Giardia species enzyme-linked immunosorbent assay (ELISA) test kit designed for use in cats was positive in three kittens. A similar test kit designed for use in humans was negative in all samples and produced negative results even when known positive samples were tested. Potentially pathogenic enteric organisms were detected in 19 kittens by routine methods and 26 (prevalence 45%) by all methods. The high prevalence in asymptomatic kittens highlights the possibility that the detection of these organisms in kittens with gastrointestinal disease may be an incidental finding.

Acute phase protein concentrations in dogs with nasal disease

The concentrations of C-reactive protein (CRP), serum amyloid A, haptoglobin (Hp) and α1-acid glycoprotein were measured in dogs with clinical signs of nasal disease and compared with those of healthy dogs in order to determine the expression of these proteins in cases of canine nasal disease. A significant difference (P<0.001) between the symptomatic group and the control group was found for both CRP and Hp. Among the animals with nasal disease, a significant intergroup difference (P<0.05) was found in the expression of Hp between dogs with aspergillosis and those with chronic rhinitis.

Hyperammonemia and systemic inflammatory response syndrome predicts presence of hepatic encephalopathy in dogs with congenital portosystemic shunts.

Hepatic encephalopathy (HE) is an important cause of morbidity and mortality in patients with liver disease. The pathogenesis of he is incompletely understood although ammonia and inflammatory cytokines have been implicated as key mediators. To facilitate further mechanistic understanding of the pathogenesis of HE, a large number of animal models have been developed which often involve the surgical creation of an anastomosis between the hepatic portal vein and the caudal vena cava. One of the most common congenital abnormalities in dogs is a congenital portosystemic shunt (cpss), which closely mimics these surgical experimental models of HE. Dogs with a cPSS often have clinical signs which mimic clinical signs observed in humans with HE. Our hypothesis is that the pathogenesis of HE in dogs with a cPSS is similar to humans with HE. The aim of the study was to measure a range of clinical, haematological and biochemical parameters, which have been linked to the development of HE in humans, in dogs with a cPSS and a known HE grade. One hundred and twenty dogs with a cPSS were included in the study and multiple regression analysis of clinical, haematological and biochemical variables revealed that plasma ammonia concentrations and systemic inflammatory response syndrome scores predicted the presence of HE. Our findings further support the notion that the pathogenesis of canine and human HE share many similarities and indicate that dogs with cPSS may be an informative spontaneous model of human HE. Further investigations on dogs with cPSS may allow studies on HE to be undertaken without creating surgical models of HE thereby allowing the number of large animals used in animal experimentation to be reduced.

Genetic data from 15 STR loci for forensic individual identification and parentage analyses in UK domestic dogs (Canis lupus familiaris)

Eighteen STR loci and one sex determination locus present in the Finnzymes Canine 2.1 STR Multiplex Reagent Kit were screened in the UK dog population providing allele frequencies and population genetic parameters necessary for the application of STRs to forensic genetic casework. A total of 375 dogs were genotyped, including representative samples from each of twelve breeds used to evaluate Hardy-Weinberg equilibrium and calculate inter-population pairwise F(ST) values. Three loci were excluded from calculations of average random match probability due to deviations from Hardy-Weinberg Equilibrium or ambiguous genotyping. Random match probability based on fifteen STR loci and one sex locus was subsequently estimated to be 2.8 × 10(-17) for unrelated individuals across breeds.

Serum cardiac troponin I in dogs with primary immune-mediated haemolytic anaemia

OBJECTIVES The assessment of serum cardiac troponin I concentrations in dogs with a range of nonprimary cardiac illnesses has revealed that cardiac myocyte damage is commonplace in many canine diseases. Whilst it is well established that dogs with fatal immune-mediated haemolytic anaemia frequently have cardiac pathology based on post-mortem examinations, there is limited information on the incidence of cardiac myocyte damage in this population of dogs. METHODS Serum cardiac troponin I concentrations were measured in 11 healthy dogs, 27 dogs with primary haemolytic anaemia and 49 hospitalised dogs without primary cardiac or haematological disorders. RESULTS Dogs with primary haemolytic anaemia have higher serum concentrations of cardiac troponin I than hospitalised ill dogs (P<0.005) and healthy dogs (P<0.01). Using a cut-off of less than 0.1 ng/mL, 20 of 27 dogs with primary haemolytic anaemia had increased serum cardiac troponin I concentrations, which was a significantly higher proportion compared to the hospitalised ill dogs (P<0.001, 16 out of 49 dogs) and healthy dogs (P<0.05, 3 out of 11 dogs). CLINICAL SIGNIFICANCE Dogs with primary haemolytic anaemia have a higher incidence of subclinical myocyte damage than healthy dogs or dogs with non-haematological or primary cardiac illnesses. The prognostic significance of increased serum cardiac troponin I concentrations in dogs with primary haemolytic anaemia merits further investigation.

Whole Blood Manganese Concentrations in Dogs with Congenital Portosystemic Shunts

BACKGROUND Manganese (Mn) is an essential mineral that is a cofactor for many enzymes required in the synthesis of proteins, carbohydrates, and lipids. Because hepatic clearance is essential in Mn homeostasis, conditions in humans resulting in hepatic insufficiency including cirrhosis and both acquired and congenital portosystemic shunting have been reported to result in increased blood Mn concentrations and increased Mn content in the central nervous system. Because Mn toxicity causes neurologic disturbances, increased Mn concentrations have been implicated in the pathogenesis of hepatic encephalopathy. HYPOTHESES Dogs with congenital portosystemic shunts (cPSS) have significantly higher whole blood Mn concentrations than do healthy dogs or those with nonhepatic illnesses. ANIMALS Eighteen dogs with cPSS, 26 dogs with nonhepatic illnesses, and 14 healthy dogs. METHODS Whole blood Mn was measured by graphite furnace atomic absorption spectrometry. The diagnosis of cPSS was made by ultrasonography or during celiotomy either by visual inspection of a shunting vessel or portovenography. RESULTS Dogs with a cPSS had significantly higher whole blood Mn concentrations than did healthy dogs and dogs with nonhepatic illnesses. Whole blood Mn concentrations were not significantly different between healthy dogs and dogs with non-hepatic illnesses. CONCLUSION AND CLINICAL IMPORTANCE Dogs with a cPSS have significantly increased whole blood Mn concentrations. Additional studies are warranted to investigate the role of Mn in cPSS-associated hepatic encephalopathy.

Calcium metabolism in eight dogs with hypoadrenocorticism

Hypoadrenocorticism is a well-described endocrinopathy in dogs that results from deficient production and secretion of glucocorticoids and/or mineralocorticoids. Although hyperkalaemia, hyponatraemia and hypochloraemia are the most common electrolyte disturbances, hypercalcaemia also occurs in approximately 30 per cent of cases. The pathogenesis of hypercalcaemia in dogs with hypoadrenocorticism is unknown. This case series reports ionised calcium, parathyroid hormone, parathyroid hormone-related protein and vitamin D metabolite concentrations that were measured in eight dogs with concurrent hypercalcaemia and hypoadrenocorticism. Ionised calcium was increased in five of seven dogs with hypercalcaemia associated with hypoadrenocorticism. Parathyroid hormone, parathyroid hormone-related protein and 1,25 dihydroxyvitamin D concentrations were within their reference ranges in seven of eight dogs, six of seven cases and six of seven dogs, respectively. This case series highlights that hypercalcaemia associated with hypoadrenocorticism is rarely associated with increases in plasma parathyroid hormone, parathyroid hormone-related protein or serum 1,25 dihydroxyvitamin D concentrations.

Low vitamin D status is associated with systemic and gastrointestinal inflammation in dogs with a chronic enteropathy

Introduction Vitamin D deficiency, as assessed by serum concentrations of 25 hydroxyvitamin D (25(OH)D), has been linked to the development of over-zealous and inappropriate inflammation in humans. However, the relationship between vitamin D status and inflammation in dogs is ill-defined. Chronic enteropathies (CE) are frequently diagnosed in client owned dogs, have a wide range of serum 25(OH)D concentrations, and represent a spontaneous model in which to probe the relationship between vitamin D and inflammation. The hypothesis of this study was that vitamin D status would be negatively associated with systemic and gastrointestinal inflammation in dogs with a CE. The aim of this study was to examine the relationship between serum 25(OH)D concentrations and markers of systemic and gastrointestinal inflammation in a cohort of dogs with CE. Methods and Materials Serum 25(OH)D concentrations, together with neutrophil, monocyte, eosinophil and lymphocyte counts, duodenal histopathology scores, serum IL-2, IL-6, IL-8 and TNFα concentrations and were measured in 39 dogs with histologically confirmed CE. A linear regression model examined the relationship between serum 25(OH)D status and measures of inflammation. Results Serum 25(OH)D concentrations were negatively associated with neutrophil and monocyte counts, duodenal histopathology scores and serum IL-2 and IL-8 concentrations. Dogs with low serum 25(OH)D concentrations typically had an inflammatory signature characterised by high monocyte and neutrophil numbers together with low lymphocyte numbers. There is a need to establish whether low vitamin D status is a cause or consequence of inflammation.