Tick paralysis in dogs and cats in Australia: treatment and prevention deliverables from 100 years of research

This review of tick paralysis caused by Ixodes holocyclus in Australia addresses the question: What are the key discoveries that have enabled effective treatment and prevention of tick paralysis in dogs and cats? Critical examination of 100 years of literature reveals that arguably only three achievements have advanced treatment and prevention of tick paralysis in animals. First, the most significant treatment advance was the commercial availability of tick antiserum in the 1930s. Hyperimmune serum currently remains the only specific anti-paralysis tick therapy available to veterinarians in Australia. Second, advances in veterinary critical care have increased survival rates of the most severely affected dogs and cats. Critical care advancements have been enabled through specialised veterinary hospitals that can provide appropriate care 24 h a day, and advanced training of veterinarians, veterinary nurses and technicians. Third, perhaps that biggest advance of all in the last 100 years of research has been the commercial availability of the isooxazoline class of acaricidal preventatives in Australia specifically for I. holocyclus. This highly effective class of preventatives offers long duration of action, low cost, spot-on or oral formulations and a low rate of adverse reactions. Animal owners and veterinarians now have the most useful tool of all – a reliable preventative. This review reveals the key events in research over the last 100 years and the tortuous pathway to delivering better treatment and preventative options for this enigmatic Australian parasite.     

New sources of resistance to Colletotrichum truncatum race Ct0 and Ct1 in Lens culinaris Medikus subsp. culinaris obtained by single plant selection in germplasm accessions

Anthracnose caused by the fungal pathogen Colletotrichum truncatum is a severe disease of lentil (Lens culinaris Medikus subsp. culinaris) causing premature defoliation and deep penetrating lesions on the stems leading to wilting and plant death. A total of 579 accessions from 20 countries were obtained from four germplasm collections in Russia, Poland, Bulgaria and Hungary. The accessions were collected between 1923 and 1988 and comprised mostly landraces. Consequently, many of the resistant entries contained susceptible plants which necessitated one or two cycles of selection of individual resistant plants for selfing and re-testing with the pathogen. Under controlled environmental conditions, plants of each accession were inoculated at early flower with C. truncatum race Ct0 (isolate 95A8) and race Ct1 (isolate 95B36), separately. Scoring of symptoms included number of lesions on the main stem, lesion penetration into the stem and amount of wilting. Resistance was obtained by single plant selection in 23 lentil accessions (4.0 %). Fifteen lines were generated with resistance to race Ct1 (2.6 %), seven with resistance to race Ct0 (1.2 %), and one line with resistance to both races. This is the first report on resistance in L. culinaris to C. truncatum race Ct0 as well as to the two races combined. Seed of homozygous resistant lines can be requested from the corresponding author, and are labeled with their original accession number with the prefix either -Ct0, -Ct1 or -Ct0Ct1 indicating resistance to one or both races of C. truncatum.     

Effect of variety and harvest date on tuber sugars and chip color

The major tuber sugars—glucose, fructose and sucrose — in tubers of the Red Pontiac, Kennebec and Monona potato varieties harvested five times during the 1970 growing season were determined quantitatively by a gas-liquid Chromatographic technique. Also, chips were made from tubers and chip color was measured objectively and reported as Rd values. Red Pontiac tubers produced the darkest-colored chips (Rd-15.5), and its tubers tended to accumulate the highest levels of the three sugars. The major difference between Monona, which produced chips with the lightest color (Rd-21.1), and Kennebec (Rd-19.5) was the very low level of glucose found in the tubers of Monona. Varieties produced chips lightest in color at the second (8/31) or third (9/15) harvest dates. Conversely, darkest-colored chips were obtained from each variety at the fourth harvest date (9/28). This was attributed to the cool, wet weather. Sugar content also varied during the harvesting schedule. Glucose content changed little until late in the season when an increase occurred. Fructose tended to decline until the final harvest when a distinct increase was obtained. Sucrose declined significantly through the third harvest, but changed little thereafter.     

The toxicity of Castanospermum australe seeds for cattle

Two calves given a mean of 16.1 g and 16.4 g ripe Castanospermum australe seeds/kg body weight daily for 13 and 16 days respectively developed haemorrhagic gastroenteritis. The first calf died. The second calf had mild myocardial degeneration and necrosis and mild nephrosis at necropsy. Two calves given a mean of 16.8 g unripe C. australe seeds/kg body weight daily for 18 days remained clinically normal and had mild gastritis at necropsy. The activity of alpha-glucosidase was reduced in the mononuclear cells of peripheral blood and in skeletal muscle. This was attributed to the presence of the indolizidine alkaloid, castanospermine, in the seeds. The toxin causing the gastroenteritis and other lesions is unknown.     

Hereditary junctional mechanobullous disease in a foal

Mechanobullous disease was diagnosed in a male Belgian foal that had sloughed hooves at 30 hours and at 6 and 12 days of age. Histologic and electron microscopic studies disclosed that lesions were the result of separation of the basal epithelial cell layer from the lamina densa of the basement membrane zone along the lamina lucida. Results of immunofluorescence on tissue specimens were negative for immunoglobulin deposition. The breeding history of the foal's dam indicated that the foal was produced from breeding of the mare to its full sibling stallion. This same mare had produced a female foal, sired by a different stallion, which also had sloughed hooves during the first 2 weeks of life and had similar histologic and electron microscopic changes. This newly recognized disease of horses most closely resembles junctional-type epidermolysis bullosa described in human beings.     

Does blood contamination of urine compromise interpretation of the urine protein to creatinine ratio in dogs?

AIMS: To determine the effect of contamination of urine with 0–5% blood, varying in haematocrit and protein concentrations, on the urine protein to creatinine ratio (UPC) in dogs, and to determine whether the colour of urine can be used to aid interpretation of UPC results.

METHODS: Urine samples were collected by free catch from 18 dogs, all of which had UPC?<0.2. Venous blood samples were also collected from each dog, and the blood from each dog was added to its own urine to produce serial concentrations of 0.125–5% blood. The colour of each urine sample was recorded by two observers scoring them as either yellow, peach, orange, orange/red or red. Protein and creatinine concentrations were determined, and dipstick analysis and sediment examination was carried out on each sample. Based on colour and dipstick analysis, samples were categorised as either having microscopic, macroscopic or gross haematuria. A linear mixed model was used to examine the effect of blood contamination on UPC.

RESULTS: The uncontaminated urine of all 18 dogs had a UPC?<0.2. Adding blood to the urine samples resulted in an increase in UPC at all contamination concentrations compared to the non-contaminated urine (p<0.001). None of the 54 samples with microscopic haematuria had UPC?>0.5. For 108 samples with macroscopic haematuria the UPC was >0.5 in 21 samples (19.4 (95% CI=13.1–27.9)%), and for 54 samples with gross haematuria 39 (72 (CI=59.1–82.4)%) had a UPC?>0.5. No samples had a UPC?>2.0 unless the blood contamination was 5% and only 3/18 (17%) samples at this blood contamination concentration had a UPC?>2.0.

CONCLUSIONS AND CLINICAL RELEVANCE: This study showed that while blood contamination of ≥0.125% does increase the UPC, if the urine remains yellow (microscopic haematuria), then there is negligible chance that a UPC?>0.5 will be solely due to the added blood. In that scenario, attributing the proteinuria present to the haematuria in the sample would be inappropriate. However blood contamination that results in discolouration of the urine sample from yellow (indicating macroscopic or gross haematuria) could increase the UPC above the abnormal range and would need to be considered as a differential for the proteinuria. Thus knowledge of urine colour, even if limited to simple colour scores (yellow, discoloured, red) could be utilised to aid interpretation of the UPC in samples with haematuria.