No abstract

Rectal swabs were collected from 147 household dogs and 35 household cats, including healthy animals, animals with gastrointestinal signs and animals with a variety of medical and surgical conditions. A combination of selective culture methods was used to optimise the recovery of Campylobacter species, and a PCR was used to confirm their isolation and to identify the species. The overall prevalence of Campylobacter species was 42.9 per cent in the cats and 41.5 per cent in the dogs. Campylobacter upsaliensis was the species most commonly isolated from the dogs and cats, and Campylobacter jejuni was the second most commonly isolated. Particularly high prevalences were detected in the few cats and dogs with diarrhoea, and in the cats and dogs that were six months old or younger.

The objectives of this study were to investigate the prevalence of food sensitivity in cats with chronic idiopathic gastrointestinal problems, to identify the food ingredients responsible, and to characterize the clinical features. Seventy cats that presented for chronic gastrointestinal signs underwent diagnostic investigation. Fifty-five cats had idiopathic problems and were entered into the study. Diagnosis of food sensitivity was made by dietary elimination-challenge studies by using commercial selected-protein diets as the elimination diet. Sixteen (29%) of the 55 cats with chronic idiopathic gastrointestinal problems were diagnosed as food sensitive. The clinical signs of another 11 cats (20%) resolved on the elimination diet but did not recur after challenge with their previous diet. The foods or food ingredients responsible for the clinical signs were dietary staples. Fifty percent of affected cats were sensitive to more than 1 food ingredient. The clinical feature most suggestive of food sensitivity was concurrent occurrence of gastrointestinal and dermatological signs. Weight loss occurred in 11 of the affected cats, and large-bowel diarrhea was more common than small-bowel diarrhea. Assay of serum antigen-specific immunoglobulin E (IgE) had limited value as a screening test, and gastroscopic food sensitivity testing was not helpful. In conclusion, adverse reactions to dietary staples were common in this population of cats, and they responded well to selected-protein diets. Diagnosis requires dietary elimination-challenge trials and cannot be made on the basis of clinical signs, routine clinicopathological data, serum antigen-specific IgE assay, gastroscopic food sensitivity testing, or gastrointestinal biopsy.

A questionnaire-based case-control study investigating the association of a range of host-related, owner-related and environmental risk factors with feline lower urinary tract disease was conducted in New Zealand over a 2-year period from 1991 to 1993. The study was subsequently extended in two ways, to examine the influence of the use of litter trays and to correlate weather records with the appearance of the disease in one particular region of the country. A range of statistical techniques was employed to analyse the data, including univariate odds ratio and chi-squared calculations, time series analysis, Poisson regression and conditional and unconditional logistic regression. Variables that were positively associated with lower urinary tract disease included low activity levels, the use of a litter tray coupled with restriction indoors, a high number of rainfall days in the month preceding the appearance of clinical signs, stress factors such as moving house within the last 3 months or the presence of more than one cat in the household, and a diet high in dry cat food. There was some indication that high levels of fluid consumption reduced the effect of a diet high in dry cat food. Other variables that appeared to have some protective effects included a routine visit to the veterinarian in the last 12 months and the use of alternative food sources such as rodents and birds.

Rectal swabs or faecal samples for the isolation of Campylobacter species were taken from 120 dogs and cats in an animal shelter in which only one kitten showed signs of gastrointestinal disease, and rectal swabs were taken from 46 dogs, 22 of which showed signs of gastrointestinal disease, in another shelter. At the first shelter, the swabs from 24 of 47 dogs (51.1 per cent) and 36 of 48 cats (75 per cent) yielded a Campylobacter species. The rate of isolation was significantly higher from dogs and cats less than six months old, and significantly higher from cats than from dogs (P< or =0.05). At the second shelter Campylobacter species were isolated from 40 of 46 dogs (87 per cent), but there was no significant difference between the age groups. Campylobacter species were isolated from 19 (86.4 per cent) of the 22 dogs with signs of gastrointestinal disease and from 21 (87.5 per cent) of the 24 unaffected dogs. Several culture methods were applied to the samples collected from both shelters, and the combination significantly increased the recovery of Campylobacter species.

Congenital hypothyroidism is a rare and underdiagnosed congenital endocrine disorder in dogs and cats and the true incidence is unknown. The disorder may cause a range of clinical signs depending on the primary defect, which affect production of thyroid hormones; some cases present when adult. Hallmark clinical signs of congenital hypothyroidism are mental impairment and skeletal developmental abnormalities, resulting in disproportionate dwarfism; goitre may or may not be present. Documented causes of congenital hypothyroidism in dogs include deficiency of, or unresponsiveness to, thyrotropin-releasing hormone (TRH) or thyroid-stimulating hormone (TSH), thyroid dysgenesis, dyshormonogenesis and iodine deficiency. In cats, TSH unresponsiveness, thyroid dysgenesis, dyshormonogenesis and iodine deficiency have been confirmed. Adequate replacement therapy results in a successful outcome in the majority of cases, especially when started early in life, as permanent developmental abnormalities can be prevented. This review describes reported cases in dogs and cats, diagnostic investigation, and recommendations for treatment.

Serum concentrations of immunoglobulin G (IgG), IgM, and IgA were measured in 9 Cavalier King Charles Spaniels with pneumonia caused by Pneumocystis sp that were examined at 4 veterinary surgeries in the United Kingdom (UK) between September 2001 and November 2002. Pneumocystis pneumonia was confirmed in all dogs by visualization of the organism in bronchoalveolar lavage fluid or a transthoracic lung aspirate. Two dogs had a history of demodicosis. Immunoglobulin concentrations also were measured in breed-and age-matched dogs sampled over the same period. IgG concentrations were significantly (P = .000) lower in the affected dogs (median 3.2 mg/mL) than in the control dogs (median 8.5 mg/mL). IgM concentrations were significantly (P = .002) higher in the affected dogs (median 1.95 mg/mL) than in the control dogs (median 1.12 mg/mL). One affected dog had no change in IgG concentration more than 3 months after resolution of infection or vaccination, but did have reduction in IgM concentration after resolution of infection and vaccination. Control dogs had low serum IgG and IgM concentrations, compared with the reference interval for all dogs. Lymphocyte count in blood was normal or high in 7 of 8 affected dogs. The results of this study suggest that there is a defect in immunity in Cavalier King Charles Spaniels that underlies the susceptibility of these dogs to pneumocystosis. Further studies are indicated to elucidate the mechanisms behind the defect, the prevalence within the breed, and the potential mode of inheritance of the problem.

Plasma TAP concentration is a good prognostic indicator in naturally occurring pancreatitis in dogs. The failure of TAP to increase in mild pancreatitis, and the increase present in severe renal disease, suggests its measurement has limited application as a sole diagnostic tool for canine pancreatitis. Further investigations are required in order to explain the large variability of urinary TAP concentration and the presence of circulating TAP in healthy dogs.