Preliminary clinical observations on the use of piroxicam in the management of rectal tubulopapillary polyps

Rectal tubulopapillary polyps were diagnosed in eight dogs following proctoscopy and mucosal pinch biopsy. Histological examination of the pinch biopsies revealed evidence of malignant transformation in three of the cases. The remaining cases were diagnosed as benign polyps. Inflammatory changes were observed in four cases. Seven dogs were treated with piroxicam suppositories and one with oral piroxicam. All dogs were re-examined after four to six weeks of piroxicam therapy and the extent of haematochezia, tenesmus and faecal mucus production was reduced in all cases. The owners of seven of the dogs considered the improvement in clinical signs to be good or excellent. Cases with and without evidence of inflammation responded equally well. This finding supports the hypothesis that piroxicam has an antineoplastic effect due to apoptosis and alteration in the cell cycle. Medical management with piroxicam may provide a non-invasive treatment option for dogs with rectal polyp formation in which surgical treatment is likely to be associated with complications such as incontinence, infection and wound breakdown, or where the owner declines such treatment.     

A sequential study of the pathology associated with the infection of sheep with adult and larval Ostertagia circumcincta

Disturbances in the physiology of the abomasa of sheep infected with either adult Ostertagia circumcincta given via abomasal cannulae, or larvae (L3) given intraruminally were matched by pathological changes in tissues collected by repeated mucosal biopsy. Within 2-3 days of the transplant of adult worms, abomasal pH had increased markedly in five out of six animals, and there also had been rapid increases in serum gastrin and pepsinogen concentrations in all animals. Reductions in parietal cell number were recorded as early as 1 day after the transplant of adults and were associated with the rapid accumulation of many neutrophils and eosinophils. Mucosal hyperplasia, with increased numbers of cells closer in appearance to mucous/mucous neck cells, was a relatively late development, being most pronounced in the latter part of the infection. In sheep given larvae, changes in secretory physiology were again matched by a concurrent fall in parietal cell number and by the accumulation of inflammatory cells. Changes became maximal when most worms could be expected to be present as adults, confirming the role of adults in the natural disease. Some abnormalities were detected in biopsies collected from animals maintained free of parasites and, although milder in degree, there were similarities to those observed in parasitised tissues, there being fewer parietal cells, a modest degree of mucous cell hyperplasia and inflammatory infiltrates of predominantly neutrophils. These changes were the likely result of trauma to the tissues in the immediate vicinity of the cannula, due either to the presence of the cannula itself or to the frequent collection of biopsy material from areas close to it.     

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.     

Hepatic lipidosis in a black-headed python (Aspidites melanocephalus).

The number of people keeping reptiles in captivity has markedly increased, and widespread inappropriate husbandry will result in an increasing incidence of the diagnosis of hepatic lipidosis(HL). It may become apparent that some species of snake have predisposition to develop HL. In the specific instance of the genus Aspidites, alterations to the usual husbandry that limit feeding and thereby body weight should markedly lessen the chance of the animal's developing HL. It is important for clinicians to develop a more aggressive approach to these cases and to build a bank of data with which to promote understanding of this common malady.     

A target-site mutation is present in a glyphosate-resistant Lolium rigidum population

Annual ryegrass (Lolium rigidum) is the only weed species to have evolved resistance to the broad‐spectrum herbicide glyphosate in Australia. A population that had failed to be controlled by glyphosate was collected from a vineyard in the Adelaide Hills region of South Australia. Dose–response experiments on this population (SLR 77) showed that it was glyphosate resistant, with an LD₅₀ that was 1.9–3.4 times higher than that of a susceptible population (VLR 1). The movement of radiolabelled glyphosate within SLR 77 plants showed that this population did not have the differential glyphosate translocation mechanism of resistance common to several other Australian glyphosate‐resistant populations. Subsequent analysis of shikimic acid accumulation within the plant after glyphosate treatment showed that this population accumulated significantly less shikimic acid than a susceptible population, but more than a glyphosate‐resistant population with the translocation mechanism, indicating the possible involvement of another mechanism of resistance. Sequencing of a portion of the SLR 77 5‐enolpyruvylshikimate‐3‐phosphate synthase gene was carried out and a mutation causing an amino acid change at position 106 from proline to threonine was identified. This mutation is likely to be responsible for glyphosate resistance in this population, as mutations in this position have been found to be responsible for glyphosate resistance in goosegrass (Eleusine indica) from Malaysia. This paper represents the first report of target‐site glyphosate resistance in L. rigidum and provides evidence that this species has at least two mechanisms of glyphosate resistance present in Australia.     

Bluetongue virus serotypes 1 and 3 infection in Poll Dorset sheep

Objective To study the clinical signs following bluetongue virus serotypes 1 and 3 infection in Poll Dorset sheep.
Design A clinical and pathological study.
Procedure Twenty Poll Dorset sheep were inoculated with bluetongue virus serotypes 1 or 3, each inoculum having a different passage history. The sheep were examined daily and their clinical appearance and rectal temperatures recorded. Heparinised and non-heparinised blood samples were taken at intervals for virological and serological study. Gross pathological findings were recorded for several sheep at necropsy and tissue samples were collected from three sheep for virological studies.
Results All inoculated sheep developed clinical disease. The clinical signs and gross pathological changes varied considerably but were consistent with damage to the vascular endothelial system. There was a decline in the titres of infectious bluetongue virus and of antigen in tissues collected between 7 and 12 days after infection.
Conclusions The severity of disease was related to the speed of onset and duration of pyrexia and not the development or titre of viraemia. Generally, those animals with sensitive mouths, depression, coronitis, recumbency and reluctance to move were the most debilitated. Whole blood was the most reliable source of infectious virus from acutely and chronically infected and convalescent animals. However, tissue samples particularly spleen, collected from dead or killed animals suffering from either peracute or acute forms of disease were most appropriate for the rapid confirmation of a clinical diagnosis.     

Clinical experience with quantitative analysis of superficial digital flexor tendon injuries in Thoroughbred and Standardbred racehorses

A method to quantitate as well as to document SDFT pathology has been described. This report indicates that computer-assisted evaluation of SDFT damage can improve the accuracy of prognosis in clinical practice. It would appear that a 3.8 severity rating is a limit past which prognosis for successful racing starts to worsen rapidly.