Alison Ridyard

Evaluation of Th1, Th2 and immunosuppressive cytokine mRNA expression within the colonic mucosa of dogs with idiopathic lymphocytic-plasmacytic colitis

The objective of this study was to evaluate the expression of the immunoregulatory and pro-inflammatory cytokines interleukin (IL)-2, IL-4, IL-6, IL-12p35, IL-12p40, interferon-gamma (IFN-gamma), and tumour necrosis factor-alpha (TNF-alpha), and the expression of the predominantly immunosuppressive cytokines transforming growth factor-beta (TGF-beta) and IL-10 in canine idiopathic lymphocytic-plasmacytic colitis (LPC). Semi-quantitative reverse transcriptase-polymerase chain reactions were performed using specific primers on RNA isolated from the colonic mucosa of healthy dogs, dogs with clinical signs of large intestinal disease but normal histopathology of the colon, and dogs with LPC. Canine LPC was associated with over-expression of IL-2 compared to healthy colonic mucosa (p<0.01) and the mucosa of dogs with large intestinal diarrhoea but normal histopathology (p<0.05). Higher levels of TNF-alpha mRNA were also seen in LPC compared to healthy mucosa (p<0.05). These results indicate that LPC is associated with activation of CD4+ T-helper lymphocytes and increased production of T-helper-1-type cytokines.

Apical Junction Complex Protein Expression in the Canine Colon: Differential Expression of Claudin-2 in the Colonic Mucosa in Dogs With Idiopathic Colitis

Canine idiopathic lymphocytic-plasmacytic colitis (LPC) is a well-recognized clinical and pathological entity in the dog, associated with altered immune cell populations and cytokine expression profiles. Clinical and experimental data indicate that alterations in the permeability of the intestinal epithelium contribute to the pathogenesis of a range of related conditions. The apical junction complex plays a significant role in regulating epithelial paracellular permeability, and we have characterized the distribution of a number of its component tight junction (ZO-1, occludin, claudin-2) and adherens junction (E-cadherin and β-catenin) proteins in normal colon and colon from dogs with idiopathic LPC. ZO-1, occludin, E-cadherin, and β-catenin exhibited a distribution in normal canine colon similar to that described previously in humans and rodents. In contrast to the situation in humans, claudin-2-specific labeling was observed in the normal canine colonic crypt epithelium, decreasing in intensity from the distal to the proximal crypt and becoming barely detectable at the luminal surface of the colon. There was little evidence for significant changes in ZO-1, occludin, E-cadherin, or β-catenin expression in dogs affected by idiopathic LPC. However, claudin-2 expression markedly increased in the proximal crypt and luminal colonic epithelium in affected dogs, suggesting a role in the pathogenesis of canine LPC. (J Histochem Cytochem 55: 1049–1058, 2007)

Evaluation of platelet activation in canine immune-mediated haemolytic anaemia

OBJECTIVES To establish whether heightened platelet activation is a common feature of canine immune-mediated haemolytic anaemia, and to evaluate the hypothesis that platelet activation plays a role in the pathogenesis of thromboembolism. METHODS Using whole-blood flow-cytometric analysis, the proportion of activated platelets and platelet-leucocyte aggregates in blood samples from 14 dogs with immune-mediated haemolytic anaemia and 14 healthy dogs was calculated. General linear models with binomial errors were used to compare groups. Results from the immune-mediated haemolytic anaemia-affected dogs were then correlated with established risk factors for thromboembolism in canine immune-mediated haemolytic anaemia, D-dimer concentration and antithrombin activity. RESULTS There was a strong correlation between platelet activation and severe thrombocytopenia, with heightened platelet activation being observed predominantly in severely thrombocytopenic dogs. CLINICAL SIGNIFICANCE Dogs with immune-mediated haemolytic anaemia, particularly those with concurrent severe thrombocytopenia, are likely to have heightened platelet activation, which may play a role in the pathogenesis of thromboembolism.

Successful Treatment of Uterine Torsion in a Cat with Severe Metabolic and Haemostatic Complications

A peri-parturient fifteen-month-old female Maine Coon cat was presented with extreme weakness and depression, profound hypovolaemia and hypothermia. Severe hyperkalaemia, hyponatraemia and anaemia were detected. Disseminated intravascular coagulation was suspected due to marked prolongation of activated partial thromboplastin time. Uterine torsion was diagnosed at exploratory laparotomy. The cat made a full recovery following ovariohysterectomy and intensive supportive therapy.

Platelet distribution width and mean platelet volume in the interpretation of thrombocytopenia in dogs

OBJECTIVE To investigate the use of platelet volume indices in the interpretation of thrombocytopenia in dogs with systemic disease. METHODS Case records of 80 control dogs and 159 thrombocytopenic dogs with systemic disease were reviewed retrospectively. The relationships between mean platelet volume, platelet distribution width and platelet count in systemically well dogs were established. Knowledge of these relationships was used to interpret thrombocytopenia in terms of the underlying disease process. RESULTS There was a positive relationship between platelet distribution width and mean platelet volume. Both platelet distribution width and mean platelet volume varied in a negative relationship with platelet count, which was unaffected by signalment, underlying disease, variations in haemotological parameters or serum proteins. CLINICAL SIGNIFICANCE The interpretation of mean platelet volume and platelet distribution width in dogs requires simultaneous reference to the platelet count. Platelet volume indices did not aid interpretation of thrombocytopenia in terms of underlying pathological processes in the population studied.

Heartworm and lungworm in dogs and cats in the UK

IN domestic carnivores, almost all parasitic diseases of the heart and lungs are caused by nematodes belonging to the Metastrongyloidea superfamily, which includes Angiostrongylus vasorum, Oslerus osleri, Filaroides species, Aelurostrongylus abstrusus and Crenosoma vulpis. The only exception is heartworm, which is caused by the filarial nematode Dirofilaria immitis. Metastrongyle infections are encountered throughout the UK, although certain geographical hot spots have been reported. While the incidence of disease associated with these parasites in dogs and cats is relatively low, largely due to the widespread use of prophylactic anthelmintics, there is anecdotal evidence that angiostrongylosis and Crenosoma infection, in particular, are on the increase. This may reflect the increasing urbanisation of the fox, which has the potential to act as a reservoir of infection. D immitis is not currently endemic in the UK and has been discussed in detail in a separate article on imported infectious diseases. This article reviews the metastrongyle infections of prime concern in this country and, for each parasite, discusses the diagnosis and management options.

Chronic gastric instability and presumed incomplete volvulus in dogs

Chronic gastric volvulus in dogs results in long-standing gastrointestinal signs unlike those of acute gastric dilatation and volvulus. This report describes chronic gastric volvulus in seven dogs. The majority of dogs presented with weight loss, chronic vomiting, lethargy and abdominal pain. A combination of radiographic, ultrasonographic and endoscopic imaging indicated altered positioning of gastric landmarks. Dynamic changes were identified in some cases. Exploratory coeliotomy and surgical gastropexy were performed in all dogs. Clinical signs improved or resolved in six of seven dogs postoperatively. Chronic gastric volvulus is an uncommon condition in dogs, but should be considered as a differential in cases presenting with the above clinical signs.

Xanthine urolithiasis in a Cavalier King Charles spaniel

XANTHINE urolithiasis is uncommon in dogs, with case series giving a prevalence of between 0.07 and 0.46 per cent (Houston and Moore 2009, Osborne and others 2009, Low and others 2010). The most common cause of canine xanthinuria is iatrogenic when allopurinol is administered, inhibiting xanthine dehydrogenase (XDH) (Bartges and Kirk 2008). In human beings, primary xanthinuria may be caused by enzyme deficiency or a cofactor abnormality. XDH deficiency may be isolated (type I), due to a missense mutation in the encoding gene for XDH, or in association with aldehyde oxidase deficiency, due to a missense mutation of the MCSU gene. Both are inherited in an autosomal recessive manner (Levartovsky and others 2000, Ichida and others 2001). Human beings with these defects may be asymptomatic with incidental hypouricaemia (Holmes and others 1974). Clinical signs, when they occur, are related to muscle deposition of xanthine causing myopathy, or renal dysfunction due to renal deposition (Nyhan 2005). A final cause of primary xanthinuria is an abnormality of the molybdenum cofactor required by xanthine oxidase, aldehyde oxidase and sulphite oxidase. Sulphite oxidase deficiency results in dramatic clinical signs of neonatal seizures and ophthalmic abnormalities (Wadman and others 1983). Xanthine uroliths appear uncommon in cats, with a prevalence of 0.1 per cent reported in uroliths submitted to the Minnesota Urolith Center, USA (Osborne and others 2004). There are case reports of xanthinuria in two domestic shorthair cats and one Himalayan cat (White and others 1997, Tsuchida and others 2007, Schweighauser and others 2009). Single nucleotide polymorphism analysis of the XDH gene in a xanthinuric Himalayan cat suggested that it had …

Thromboembolism in Dogs with Protein-Losing Enteropathy with Non-Neoplastic Chronic Small Intestinal Disease.

Dogs with protein-losing enteropathy (PLE) are suggested to be at increased risk of developing thromboembolic events. However, with some exceptions, there are very few reports of thromboembolism in such dogs. This multicentre retrospective observational study describes a case series of thromboembolism (TE) in eight dogs with PLE secondary to non-neoplastic, chronic small intestinal disease. Seven dogs had poorly controlled PLE when the thromboembolic event occurred. Pulmonary thromboembolism (PTE) occurred in six dogs, while one dog developed splenic vein thrombosis and another had concurrent splenic vein and aortic TE. Six dogs died, all with PTE. Antithrombin activity was decreased in one of two dogs in which it was measured. Serum cobalamin and folate concentrations were measured in three dogs and cobalamin was subnormal in all three. Serum magnesium, measured in two dogs, was low in both. Dogs with uncontrolled chronic small intestinal disease and PLE are at risk for developing serious life-threatening TE, mostly PTE.