Arterial Thromboembolism in 250 Cats in General Practice: 2004–2012

Background

Population characteristics and outcome of cats with arterial thromboembolism (ATE) managed in general practice (GP) have been poorly described.

Hypothesis

Cats with ATE presenting to GP are usually euthanized at presentation, but survival times >1 year are possible.

Animals

Cats with ATE managed by 3 GP clinics in the United Kingdom.

Methods

Records of cases presenting to GP over a 98‐month period (2004–2012) were reviewed. Cats with an antemortem diagnosis of limb ATE were included. Outcome information was obtained.

Results

Over 98 months, 250 cats were identified with ATE. Prevalence was approximately 0.3%. At presentation, 153 cats (61.2%) were euthanized, with 68/97 (70.1%) of the remaining cats (27.2% of the total population) surviving >24 hours after presentation. Of these, 30/68 (44.1%) survived for at least 7 days. Hypothermia (HR, 1.44; 95% CI, 1.002–2.07; P = .049) and management by Clinic 2 (HR, 5.53; 95% CI, 1.23–24.8; P = .026) were independent predictors of 24‐hour euthanasia or death. For cats surviving >24 hours, hypothermia (HR, 2.25; 95% CI, 1.12–4.48; P = .021) and failure to receive aspirin, clopidogrel, or both (HR, 8.26; 95% CI, 1.39–50; P = .001) were independent predictors of euthanasia or death within 7 days. For cats that survived ≥7 days, median survival time was 94 (95% CI, 42–164) days, with 6 cats alive 1 year after presentation.

Conclusions

Although 153/250 cats were euthanized at presentation, 6 cats survived >12 months. No factors were identified that predicted euthanasia on presentation.     

Predictors of Clinical Remission in Cats with Diabetes Mellitus

Background: Clinical remission is frequent in cats with well‐controlled diabetes mellitus, but few studies explored predictors of this phenomenon. Hypothesis: Data retrieved from medical records at admission might be valuable to identify likelihood of remission and its duration in diabetic cats. Animals: Ninety cats with newly diagnosed diabetes, followed‐up until death or remission. Methods: Retrospective cohort study. Data were collected from records at admission, including history, signalment, physical examination, haematology, and biochemical profile, and the occurrence and duration of remission, defined as normoglycemia without insulin for ≥4 weeks. Predictors of remission were studied with univariate and multivariate logistic regression. Factors associated with remission duration were analyzed with Kaplan‐Meier and Cox proportional hazard models. Results: Forty‐five (50%) cats achieved remission, after a median time of 48 days (range: 8–216). By study end, median remission duration was 114 days (range: 30–3,370) in cats that died and 151 days (range: 28–1,180) in alive cats. Remission was more likely with higher age (OR: 1.23, 95% CI: 1.04–1.46; P= .01) and less likely with increased serum cholesterol (OR: 0.36, 95% CI: 0.11–0.87; P= .04). Remission was longer with higher body weight (HR: 0.65, 95% CI: 0.42–0.99; P= .04) and shorter with higher blood glucose (HR: 1.01, 95% CI: 1.00–1.02; P= .02). Conclusions and Clinical Importance: Age, body weight, cholesterol, and glucose levels are suggested for prediction of remission or its duration in diabetic cats. Older cats developing diabetes may have a better outcome, possibly suggesting a slower disease progression.     

Risk factors for time to diagnosis of feline upper respiratory tract disease in UK animal adoption shelters

Feline upper respiratory tract disease (URTD), mainly caused by feline calicivirus (FCV) and feline herpesvirus, is a major cause of disease outbreaks in feline accommodation such as animal shelters, catteries and multi-cat households. We conducted a longitudinal, yearlong study in five UK feline animal shelters to identify risk factors for the time to diagnosis of URTD. We were especially interested in risk factors that could be identified at the time the cat entered the shelter. Shelter staff recorded data for 1434 cats during 2002–2003. Most of the cats were domestic shorthair cats and were from private households, or were stray or abandoned. Sixty cats without clinical signs of URTD at entry had URTD diagnosed (typically within the first month at the centre). We used two multivariable models: one was a Cox proportional-hazards model, and the other a regression analyses with complementary log–log model.The hazard varied substantially between shelters and was considerably lower for the shelter that had a purpose-built admissions unit with its own isolation facilities. The hazard was greater for purebred cats (HR 4.3–5.0) and for neutered cats (HR 2.0). The hazard was also typically greater if the centre had a greater proportion of cats present with URTD. The analyses suggested that the centre-level risk factors were more important in determining hazard than cat-level risk factors.     

Onset of immunity in kittens after vaccination with a non-adjuvanted vaccine against feline panleucopenia, feline calicivirus and feline herpesvirus

The induction of a quick onset of immunity against feline parvovirus (FPV), feline herpesvirus (FHV) and feline calicivirus (FCV) is critical both in young kittens after the decline of maternal antibodies and in cats at high risk of exposure. The onset of immunity for the core components was evaluated in 8–9 week old specific pathogen free kittens by challenge 1 week after vaccination with a combined modified live (FPV, FHV) and inactivated (FCV) vaccine. The protection obtained 1 week after vaccination was compared to that obtained when the challenge was performed 3–4 weeks after vaccination. The protocol consisted of a single injection for vaccination against FPV and two injections 4 weeks apart for FHV and FCV.At 1 week after vaccination, the kittens showed no FPV-induced clinical signs or leukopenia following challenge, and after FCV and FHV challenges the clinical score was significantly lower in vaccinated animals than in controls. Interestingly, the relative efficacy of the vaccination was comparable whether the animals were challenged 1 week or 3–4 weeks after vaccination, indicating that the onset of protection occurred within 7 days of vaccination. Following the 1-week challenge, excretion of FPV, FHV and FCV was significantly reduced in vaccinated cats compared to control kittens, confirming the onset of immunity within 7 days of vaccination.     

Is the metabolic syndrome a useful clinical concept in dogs? A review of the evidence

The metabolic syndrome is a set of risk factors for the development of type 2 diabetes, atherosclerosis, coronary heart disease and stroke in human beings. The term has recently been applied to dogs that exhibit components of the human metabolic syndrome, specifically visceral obesity, hypercholesterolaemia, hypertriglyceridaemia, hypertension and fasting hyperglycaemia. Obese dogs, like obese humans, are known to develop resistance to the glucose-lowering effects of insulin, and develop increased circulating concentrations of triglycerides, cholesterol and blood pressure. Unlike humans, however, obese dogs do not develop fasting hyperglycaemia or atherogenic hyperlipidaemia. Importantly, there is no evidence that dogs develop type 2 diabetes. Atherosclerosis, coronary heart disease and stroke are rare and not known to be associated with obesity in dogs. On the basis of current knowledge, the use of the term ‘metabolic syndrome’ in dogs does not appear to have merit.     

豹源猫杯状病毒ORF2基因的扩增、克隆及原核表达

为制备猫杯状病毒血清学检测抗原,本研究根据实验室保存的1株豹源猫杯状病毒基因序列设计引物,扩增了开放阅读框2（ORF2）中1734 bp的核苷酸序列,将其克隆至表达载体pET-28a上,构建了pET-28a-FCV1734重组质粒。将该质粒转化大肠杆菌,诱导表达产物经SDS-PAGE和Western blot检测,证明所表达的蛋白具有良好的反应原性。     

Helicobacter infection in dogs and cats: facts and fiction

The discovery of the spiral bacterium Helicobacter pylori and its causative role in gastric disease in humans has brought a dramatic change to gastroenterology. Although spiral bacteria have been known for more than a century to infect the stomachs of dogs and cats, recent research has been conducted mainly in the wake of interest in H. pylori. H. pylori has not been found in dogs and only very rarely in cats and zoonotic risk is minimal. A variety of other Helicobacter spp. can infect the stomach of pets; however, their pathogenic role is far from clear, and they have a small but real zoonotic potential. The prevalence of gastric Helicobacter spp. in dogs and cats is high, irrespective of clinical signs, and as in human medicine, mode of transmission is unclear. The relationship of Helicobacter spp. to gastric inflammation in cats and dogs is unresolved, with inflammation, glandular degeneration, and lymphoid follicle hyperplasia accompanying infection in some but not all subjects. Circulating anti-Helicobacter immunoglobulin G antibodies have been detected in 80% of dogs with naturally acquired infection and most dogs and cats with experimental infection. The gastric secretory axis is similar in infected and uninfected cats and dogs and no relationship of infection to gastrointestinal ulcers has been found. Differences in the pathogenicity of Helicobacter spp. are apparent, because infection with H pylori is associated with a more severe gastritis than infection with other Helicobacter spp. in both cats and dogs. Rapid urease test, histopathology, and touch cytology are all highly accurate invasive diagnostic tests for gastric Helicobacter-like organisms in dogs and cats, whereas culture and polymerase chain reaction are the only means to identify them to the species level. Urea breath and blood tests or serology can be used to diagnose Helicobacter spp. noninvasively in dogs and cats. Most therapeutic studies in pets have not shown long-term eradication of Helicobacter spp. Whether this is due to reinfection or recrudescence has not been established.     

Simultaneous detection of the feline lungworms Troglostrongylus brevior and Aelurostrongylus abstrusus by a newly developed duplex-PCR

In addition to Aelurostrongylus abstrusus (Strongylida: Angiostrongylidae), referred to as the feline lungworm, Troglostrongylus brevior (Strongylida: Crenosomatidae) has recently been identified as an agent of bronco-pulmonary infestations in cats. These two parasites have a similar biology, share ecological niches, potentially co-infesting cats, but are difficult to be differentiated due to the morphological similarities of their first-stage larvae (L1). This paper describes a molecular tool, based on single-step duplex polymerase chain reaction (duplex-PCR) on the ribosomal internal transcribed spacer 2 region (ITS-2) for the simultaneous detection and differentiation of T. brevior and A. abstrusus. L1 of both species were collected from faecal samples, morphologically identified, and single larval specimens isolated. An aliquot of faeces was used as a test sample for a case of mixed natural infestation. The duplex-PCR was performed using species-specific forward primer sets for the ITS-2 region (i.e., A. abstrusus: 220 bp; T. brevior: 370 bp). The detection limit of the molecular assay was also assessed by serial dilutions of DNA from single larvae of both species (from ～4.0 to 4.0 × 10^?5 μg/μl). The duplex-PCR carried out on individual DNA samples was able to detect as low as 5.2 × 10^?3 μg/μl of DNA for A. abstrusus, 4.9 × 10^?3 μg/μl for T. brevior, and as low as 4.0 × 10^?3 μg/μl for samples containing both species. Species-specific bands of the expected sizes and two bands were simultaneously amplified from the faecal sample containing both species. The phylogenetic analyses of the ITS-2 sequences here examined and those available for other metastrongyloids were concordant in clustering them with those of other Troglostrongylus brevior and A. abstrusus sequences available in GenBank database. This molecular approach proved to be effective and highly sensitive for the simultaneous detection of the two lungworms species and it might be used for molecular epidemiological studies and for monitoring therapeutic protocols.     

Characterization of the gut microbiota in leptin deficient obese mice – Correlation to inflammatory and diabetic parameters

Gut microbiota have been implicated as a relevant factor in the development of type 2 diabetes mellitus (T2DM), and its diversity might be a cause of variation in animal models of T2DM. In this study, we aimed to characterise the gut microbiota of a T2DM mouse model with a long term vision of being able to target the gut microbiota to reduce the number of animals used in experiments. Male B6.V-Lep^ob/J mice were characterized according to a number of characteristics related to T2DM, inflammation and gut microbiota. All findings were thereafter correlated to one another in a linear regression model. The total gut microbiota profile correlated to glycated haemoglobin, and high proportions of Prevotellaceae and Lachnospiraceae correlated to impaired or improved glucose intolerance, respectively. In addition, Akkermansia muciniphila disappeared with age as glucose intolerance worsened. A high proportion of regulatory T cells correlated to the gut microbiota and improved glucose tolerance. Furthermore, high levels of IL-10, IL-12 and TNF-α correlated to impaired glucose tolerance, blood glucose or glycated haemoglobin. The findings indicate that gut microbiota may contribute to variation in various disease read-outs in the B6.V-Lep^ob/J model and considering them in both quality assurance and data evaluation for the B6.V-Lep^ob/J model may have a reducing impact on the inter-individual variation.     

猫鼻气管炎病毒、怀状病毒、泛白细胞减少症病毒的分离及其其形态学观察

根据病毒的理化特性,从猫三联活疫苗中分离出猫鼻气管炎、猫西洋太和猫泛白细胞减少症病毒;筛选出每种病毒敏感的细胞,并将该3种病毒分别分别在其中传代与扩增;通过电镜观察此3种病毒的形态学特征及其在宿主细胞内增殖部位、分布情况等,并以此对猫3种病毒进行了初步鉴定。     

Can heartworm prevalence in dogs be used as provisional data for assessing the prevalence of the infection in cats?

Cats are considered a susceptible host for Dirofilaria immitis; however, increased host resistance is reflected by relatively low adult worm burdens in natural and experimental infections; the prolonged prepatent period (8 months); the low level and short duration of microfilaremia; and the short life span of adult worms (2-3 years). From April to September 2006, 212 cats and 608 dogs, all exposed for at least one transmission season, were screened for D. immitis infection in a multi-center study in the Po River Valley in northern Italy. Cats were initially evaluated by antibody testing; positive subjects were followed up by antigen testing and echocardiography (and necropsy if death occurred). The prevalence in dogs was 29% by a modified Knott test and antigen testing compared with a prevalence of 4.7% in cats by an antibody test; six of these infections (2.8%) were confirmed by the follow-up evaluations. This field study demonstrated that the prevalence of heartworm infection in cats in this area is within the expected limits of 9-18% of the prevalence in dogs. Antibody testing likely underestimates the real prevalence of D. immitis infection in cats. These results also emphasize the importance of preventive treatment in cats.     

Compensation for obesity-induced insulin resistance in dogs: assessment of the effects of leptin, adiponectin, and glucagon-like peptide-1 using path analysis

The hormonal mediators of obesity-induced insulin resistance and compensatory hyperinsulinemia in dogs have not been identified. Plasma samples were obtained after a 24-h fast from 104 client-owned lean, overweight, and obese dogs. Plasma glucose and insulin concentrations were used to calculate insulin sensitivity and β-cell function with the use of the homeostasis model assessment (HOMA_{insulin sensitivity} and HOMA_{β-cell function}, respectively). Path analysis with multivariable linear regression was used to identify whether fasting plasma leptin, adiponectin, or glucagon-like peptide-1 concentrations were associated with adiposity, insulin sensitivity, and basal insulin secretion. None of the dogs were hyperglycemic. In the final path model, adiposity was positively associated with leptin (P < 0.01) and glucagon-like peptide-1 (P = 0.04) concentrations. No significant total effect of adiposity on adiponectin in dogs (P = 0.24) was observed. If there is a direct effect of leptin on adiponectin, then our results indicate that this is a positive relationship, which at least partly counters a negative direct relationship between adiposity and adiponectin. Fasting plasma leptin concentration was directly negatively associated with fasting insulin sensitivity (P = 0.01) and positively associated with β-cell function (P < 0.01), but no direct association was observed between adiponectin concentration and either insulin sensitivity or β-cell function (P = 0.42 and 0.11, respectively). We conclude that dogs compensate effectively for obesity-induced insulin resistance. Fasting plasma leptin concentrations appear to be associated with obesity-associated changes in insulin sensitivity and compensatory hyperinsulinemia in naturally occurring obese dogs. Adiponectin does not appear to be involved in the pathophysiology of obesity-associated changes in insulin sensitivity.