Companion animal cancer diagnostic reports are text-based documents containing essential information on tumor classification and diagnosis. Establishing an animal cancer registry requires integrating and extracting structured data from diverse report formats across multiple providers. This study presents the development of an object-oriented programming approach to standardize and automate cancer data collection for canine and feline patients, enabling the creation of the Australian Companion Animal Registry of Cancers (ACARCinom); Australia's first national registry of cat and dog cancers. An object-oriented programming approach was developed using the C# language for data processing, tested on sample data from 6 data providers. The initial programming phase focused on designing a parser that identified report sections using regular expressions based on standardized headings. The text was then cleaned to remove unnecessary formatting and HTML tags. Data dictionaries containing preferred terms and synonyms were used to extract key information such as diagnosis, topography, grade, and metastasis, improving consistency and accuracy. A coordinate map of extracted terms was generated to analyze spatial relationships within the report, allowing prioritization of diagnoses. The system also logged parsing decisions and potential issues for expert review. Markup using HTML tags enabled clear visualization of parsed content within the original reports. Extracted data and patient metadata were stored in an intermediary database table, allowing veterinary pathology experts to review and refine entries before final import. This automated solution streamlines data extraction and standardization from diverse sources, enabling the efficient analysis of cancer records and enhancing research and surveillance capacity in veterinary oncology.

Veterinary RecordVolume 193, Issue 1 p. 31-33 Research comment What clinicopathological factors predict prognosis for canine subcutaneous mast cell tumours? Anne Peaston, Corresponding Author Anne Peaston [email protected] School of Animal and Veterinary Sciences, University of Adelaide, Roseworthy, South Australia, AustraliaSearch for more papers by this author Anne Peaston, Corresponding Author Anne Peaston [email protected] School of Animal and Veterinary Sciences, University of Adelaide, Roseworthy, South Australia, AustraliaSearch for more papers by this author First published: 07 July 2023 https://doi.org/10.1002/vetr.3237Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. References 1London CA, Thamm DH. Mast cell tumors. In: DM Vail, DH Thamm, JM Liptak, eds. Withrow and MacEwen's Small Animal Clinical Oncology, 6th Edition. St Louis: Saunders, 2020: 382–403 2Bostock DE. The prognosis following removal of mastocytomas in dogs. J Small Anim Pract 1973; 14: 27–41 3Patnaik AK, Ehler WJ, MacEwen EG. Canine cutaneous mast cell tumor: morphologic grading and survival time in 83 dogs. Vet Pathol 1984; 21: 469–74 4Kiupel M, Webster JD, Bailey KL, et al. Proposal of a 2-tier histologic grading system for canine cutaneous mast cell tumors to more accurately predict biological behavior. Vet Pathol 2011; 48: 147–55 5Newman SJ, Mrkonjich L, Walker KK, et al. Canine subcutaneous mast cell tumour: diagnosis and prognosis. J Comp Pathol 2007; 136: 231–9 6Thompson JJ, Pearl DL, Yager JA, et al. Canine subcutaneous mast cell tumor: characterization and prognostic indices. Vet Pathol 2011; 48: 156–68 7Gill V, Leibman N, Monette S, et al. Prognostic indicators and clinical outcome in dogs with subcutaneous mast cell tumors treated with surgery alone: 43 cases. J Am Anim Hosp Assoc 2020; 56: 215–25 8Camus MS, Priest HL, Koehler JW, et al. Cytologic criteria for mast cell tumor grading in dogs with evaluation of clinical outcome. Vet Pathol 2016; 53: 1117–23 9Marconato M, Stefanello D, Solari Basano F, et al. Subcutaneous mast cell tumours: a prospective multi-institutional clinicopathological and prognostic study of 43 dogs. Vet Rec 2023; doi: 10.1002/vetr.2991 10Weishaar KM, Thamm DH, Worley DR, et al. Correlation of nodal mast cells with clinical outcome in dogs with mast cell tumour and a proposed classification system for the evaluation of node metastasis. J Comp Pathol 2014; 151: 329–38 11Thompson JJ, Yager JA, Best SJ, et al. Canine subcutaneous mast cell tumors: cellular proliferation and kit expression as prognostic indices. Vet Pathol 2011; 48: 169–81 Volume193, Issue18/15 July 2023Pages 31-33 ReferencesRelatedInformation

Antigenic differences between commercial Newcastle Disease Virus (NDV) vaccine and circulating field virus reduce vaccine efficacy. Fifty-layer chickens were divided into five groups: three vaccinated chicken groups using killed LaSota (Genotype II/GII), Mega, or VD (Genotype VII/GVII) viral strains, negative, and positive control groups. On day 28, Hemagglutination Inhibition (HI) serology of vaccinated chickens was performed using whole virus antigens of RIVS, LaSota, Mega, and VD strains. Sera were also tested with an alternative antigen, using an ELISA to detect antibody for the cleavage site F protein peptide from GII and GVII NDV strains. Vaccinated and unvaccinated positive control birds underwent infectious challenges using VD and Mega strains. HI testing showed that antibody titers were higher when tested using homologous antigens than heterologous antigens. ELISA performed with alternative antigens did not perform as well as the established HI test using homologous strains. Viral shedding was reduced by vaccination that was homologous to the infectious challenge in comparison with vaccination using the LaSota strain virus. We conclude that superior results are obtained when serological testing, vaccinations, and vaccine challenge experiments all use circulating strains of ND virus. Implementation of this recommendation would likely reduce viral shedding by vaccinated chickens and be more effective in preventing outbreaks of virulent NDV.

Abstract Background Dogs have a species‐specific susceptibility for developing mast cell tumours (MCTs). Mutations in the KIT proto‐oncogene (KIT) are known to contribute to the neoplastic biology of mast cells. In dogs, the most common KIT mutation is an internal tandem duplication (ITD) in exon 11 which has been considered a useful prognostic supplement to traditional histopathological tumour grading. Objective The aim of this retrospective study was to explore the importance of KIT exon 11 ITD mutation status and known clinical and pathological indices in predicting prognosis in a cohort of Australian dogs diagnosed with MCT. Methods Clinical parameters, survival data, and KIT mutation status were collected and assessed for 220 dogs with cutaneous or subcutaneous MCT (n = 189 and n = 31, respectively). Results In at least one of the multivariable models, tumour grade (cutaneous Kiupel low or high grade) or tumour subcutaneous location, multiple concurrent MCTs, metastasis at the time of surgery, and senior age were statistically significant in predicting the outcome (MCT‐related death and/or second MCT diagnosis) at 6‐ or 12‐month post‐tumour excision. KIT exon 11 ITD mutation status was not a significant predictor in any of the final multivariable models and was strongly correlated with high histological grade (p < 0.001). Conclusion In this sample of dogs, tumour histological grading remained the single most powerful prognostic indicator for MCT outcome. However, concurrent evaluation of multiple prognostically significant parameters provides information of potential value to inform therapeutic management for each patient.

Mast cell tumours (MCT) have been documented in numerous species and mutations within the KIT proto-oncogene are implicated in the neoplastic biology of mast cells in humans, dogs and cats. This study determined high KIT gene nucleotide and Kit amino acid sequence homology between several species known to suffer mast cell neoplasia and especially high sequence conservation between the cheetah (Acinonyx jubatus) and domestic cat (Felis catus) KIT sequences. As a result, we hypothesised that KIT mutations would exist in the neoplastic DNA of four cheetahs diagnosed with MCT from a recent case series. PCR and Sanger sequencing identified conservative exon 6 KIT mutations in two of the four cheetahs. The mutations were different between the two cheetahs. Only wild-type DNA in exons 6, 8, 9 and 11 of KIT was observed in the MCTs of the remaining two cheetahs. Twenty cutaneous MCTs from domestic cats were collected for KIT mutation comparison. Twelve tumours possessed a mutation within KIT exons 6, 8 or 9 (60%, 95% CI 38.5%-81.5%). No mutations were detected in exon 11. There was no significant association between domestic feline MCT KIT mutation status and tumour histological grade (traditional schematic, P = .934; Sabattini 2-tier schematic, P = .762) or mitotic index (P = .750). KIT mRNA and Kit protein sequences are conserved across species but the role of KIT in feline MCT pathogenesis is not completely understood.

In this study, three different diagnostic tests for parvovirus were compared with vaccination status and parvovirus genotype in suspected canine parvovirus cases. Faecal samples from vaccinated (N17) and unvaccinated or unknown vaccination status (N41) dogs that had clinical signs of parvovirus infection were tested using three different assays of antigen tests, conventional and quantitative PCR tests. The genotype of each sample was determined by sequencing. In addition to the suspected parvovirus samples, 21 faecal samples from apparently healthy dogs were tested in three diagnostic tests to evaluate the sensitivity and specificity of the tests. The antigen test was positive in 41.2% of vaccinated dogs and 73.2% of unvaccinated diseased dogs. Conventional PCR and qPCR were positive for canine parvovirus (CPV) in 82.4% of vaccinated dogs and 92.7% of unvaccinated dogs. CPV type-2c (CPV-2c) was detected in 82.75% of dogs (12 vaccinated and 36 unvaccinated dogs), CPV-2b was detected in 5.17% dogs (one vaccinated and two unvaccinated) and CPV-2a in 1.72% vaccinated dog. Mean Ct values in qPCR for vaccinated dogs were higher than the unvaccinated dogs (p = 0.049), suggesting that vaccinated dogs shed less virus, even in clinical forms of CPV. CPV-2c was the dominant subtype infecting dogs in both vaccinated and unvaccinated cases. Faecal antigen testing failed to identify a substantial proportion of CPV-2c infected dogs, likely due to low sensitivity. The faecal samples from apparently healthy dogs (n = 21) showed negative results in all three tests. Negative CPV faecal antigen results should be viewed with caution until they are confirmed by molecular methods.

Osteosarcoma is the most common paediatric primary bone malignancy. The major cause of death in osteosarcoma is drug-resistant pulmonary metastasis. Previous studies have shown that thioredoxin reductase 2 is a driver of metastasis in osteosarcoma and can be inhibited by auranofin (AF). Moreover, studies have shown that AF significantly reduces pulmonary metastases in xenotransplant models. Here, we describe a phase I/II study of AF in canine osteosarcoma, a well-recognized spontaneous model of human osteosarcoma. We performed a single-arm multicentre pilot study of AF in combination with standard of care (SOC) (amputation + carboplatin). We recruited 40 dogs to the trial and used a historical SOC-only control group (n = 26). Dogs >15 kg received 9 mg AF q3d PO and dogs <15 kg received 6 mg q3d. Follow-up occurred over at least a 3-year period. Auranofin plus SOC improved overall survival (OS) (P = .036) in all dogs treated. The improved outcome was attributable entirely to improved OS in male dogs (P = .009). At the time of writing, 10 dogs (25%) survive without measurable disease in the treatment group with survival times ranging between 806 and 1525 days. Our study shows that AF improves OS in male dogs when combined with SOC. Our findings have translational relevance for the management of canine and human osteosarcoma. Our data justify a larger multicentre phase 2 trial in dogs and a phase I/II trial in human patients with refractory disease at the time of initial surgery.

The full-genome sequences of strains chicken/Indonesia/Cilebut/010WJ/2015 and chicken/Indonesia/ITA/012WJ/1951, isolated in West Java, Indonesia, in 2015 and 1951, respectively, were examined. Chicken/Indonesia/Cilebut/010WJ/2015 (genotype VII) caused a 2015 disease outbreak in Indonesia, and chicken/Indonesia/ITA/012WJ/1951 (genotype VI) is used as a standard strain for challenge in Newcastle disease virus (NDV) vaccine trials.

Mast cell tumors in nondomestic felids are rarely reported and their biological characteristics are not well described. A retrospective review of the pathology records of 52 zoo-housed cheetahs (Acinonyx jubatus) identified five cases of mast cell tumor, involving four closely related individuals. The age at initial presentation varied from 14 mo to 6 yr. Four cases presented as solitary or multiple cutaneous masses that were mostly slow growing, up to 20 mm diameter, and predominantly nonulcerated. The diagnosis was made by fine needle aspiration cytology of a lesion in one case and by excisional biopsy in the others. Histopathologically, the lesions resembled low- to intermediate-grade canine mast cell tumors, with variations in the degree of anisocytosis and anisokaryosis. Surgical excision was incomplete for 80% of the cutaneous lesions, but local recurrence was not observed in any case. One animal with cutaneous lesions subsequently developed fatal visceral mastocytosis involving the spleen, liver, and adrenal gland. There was no evidence of lymph node invasion or paraneoplastic gastrointestinal signs in any of the cases.

Mast cell neoplasia clinical presentation and biological behaviour vary considerably across mammalian species, ranging from a solitary benign mass to an aggressive systemic malignancy. Mutations in the KIT Proto-Oncogene Receptor Tyrosine Kinase (KIT) gene are common molecular abnormalities involved in mast cell tumorigenesis. KIT mutations often occur in dog, cat and human neoplastic mast cells and result in altered Kit protein structure and function. In dogs, certain KIT mutations are associated with more malignant and lethal disease. In contrast, KIT mutations in feline and human mast cell neoplasms are not correlated with prognosis, but are of value in diagnosis and treatment planning in humans. KIT genetic abnormalities have not been well investigated in other species, although aberrant cytoplasmic Kit protein staining detected in neoplasms of the ferret, horse and cow resembles aberrant Kit staining patterns detected in neoplastic mast cells of dogs, cats and humans. Mutations within KIT are classified as either regulatory-type or enzymatic pocket-type mutations according to their location within the KIT Proto-Oncogene. Mutations within the enzymatic pocket domain confer tumour resistance to tyrosine kinase inhibitors (TKIs). Hence, knowledge of tumour KIT mutation status adds valuable information for optimizing patient treatment strategies. The use of TKIs in combination with conventional chemotherapeutics has opened a new treatment avenue for patients unresponsive to existing drugs. This review highlights the similarities and differences of mast cell neoplasia in mammals with a special focus on the involvement of KIT in the canine and feline forms in comparison to human mast cell neoplasia.

Little is known about genetic causes of congenital methemoglobinemia in dogs. Here, we report a CYB 5 R 3 mutation in a Pomeranian dog with congenital methemoglobinemia. A 6-year-old neutered female Pomeranian dog was investigated for cyanosis noticed during anesthesia for an orthopedic procedure. The history included lifelong mild exercise intolerance and bluish tongue. Methemoglobinemia was diagnosed using co-oximetry. The CYB 5 R 3 gene was analyzed by comparing the patient's genomic DNA with the reference canine sequence. Mutation functional significance was investigated using snpEff and multispecies protein homology analyses. A homozygous missense single nucleotide CYB 5 R 3 mutation (ATC ➔ CTC at codon 194) caused a p.Ile194Leu substitution. The pIle194 residue is highly conserved in other mammals, supporting the likely pathogenicity of the substitution. The mutation described here is identical to that associated with familial methemoglobinemia in a family of Japanese Pomeranian dogs. This observation, together with the homozygous mutation found in our case, indicates that the mutant allele may be widespread within the Pomeranian breed internationally.

Little is known about genetic causes of congenital methemoglobinemia in dogs. Here, we report a CYB 5 R 3 mutation in a Pomeranian dog with congenital methemoglobinemia. A 6‐year‐old neutered female Pomeranian dog was investigated for cyanosis noticed during anesthesia for an orthopedic procedure. The history included lifelong mild exercise intolerance and bluish tongue. Methemoglobinemia was diagnosed using co‐oximetry. The CYB 5 R 3 gene was analyzed by comparing the patient's genomic DNA with the reference canine sequence. Mutation functional significance was investigated using snpEff and multispecies protein homology analyses. A homozygous missense single nucleotide CYB 5 R 3 mutation (ATC ➔ CTC at codon 194) caused a p.Ile194Leu substitution. The pIle194 residue is highly conserved in other mammals, supporting the likely pathogenicity of the substitution. The mutation described here is identical to that associated with familial methemoglobinemia in a family of Japanese Pomeranian dogs. This observation, together with the homozygous mutation found in our case, indicates that the mutant allele may be widespread within the Pomeranian breed internationally.

In Australia, compulsory microchipping legislation requires that animals are microchipped before sale or prior to 3 months in the Australian Capital Territory, New South Wales, Queensland and Victoria, and by 6 months in Western Australia and Tasmania. Describing the implementation of microchipping in animals allows the data guardians to identify individual animals presenting to differing veterinary practices over their lifetimes, and to evaluate compliance with legislation. VetCompass Australia (VCA) collates electronic patient records from primary care veterinary practices into a database for epidemiological studies. VCA is the largest companion animal clinical data repository of its kind in Australia, and is therefore the ideal resource to analyse microchip data as a permanent unique identifier of an animal. The current study examined the free-text ‘examination record’ field in the electronic patient records of 1000 randomly selected dogs and cats in the VCA database. This field may allow identification of the date of microchip implantation, enabling comparison with other date fields in the database, such as date of birth. The study revealed that the median age at implantation for dogs presented as individual patients, rather than among litters, was 74.4 days, significantly lower than for cats (127.0 days, p = 0.003). Further exploration into reasons for later microchipping in cats may be useful in aligning common practice with legislative requirements.

DNA amplification by PCR detects KIT exon 11 internal tandem duplications in canine mast cell tumors (MCTs). Tissue-specific inhibitors often contaminate DNA extracted from formalin-fixed, paraffin-embedded (FFPE) canine MCTs, blocking PCR amplification and, consequently, preventing mutation detection. We used a commercial kit to extract DNA from FFPE canine MCTs. Two independent PCR assays, each with one primer set, were used to amplify target genes (HPRT and KIT) directly after FFPE DNA extraction. PCR amplification failed with at least one primer set in 153 of 280 samples (54.6%, 95% CI: 48.8-60.5%). One or 2 DNA washing steps were required to remove PCR inhibitors in 130 of 280 (46.4%) and 23 of 280 (8.2%) of these cases, respectively. DNA concentration and quality (A260/A280 and A260/A230) either pre- or post-washing were not associated with ability of the samples to be amplified by PCR using both HPRT and KIT primer sets. Low-grade and subcutaneous MCTs were less likely to amplify directly after DNA extraction and without any washing steps compared to high-grade MCTs using KIT gene primers.

The aim of the study was to develop a quantitative real-time PCR assay for diagnosis and monitoring of mycoplasma urinary tract infections (UTI) in a dog. An English Cocker Spaniel dog with the history of urinary tract infection was physically examined and laboratory findings identified chronic renal insufficiency and urinary tract infection. Attempts to culture organisms from pyuric urine failed, and empirical antibiotic therapy did not resolve the pyuria. A mycoplasma species most closely resembling Ureaplasma canigenitalium was identified in urine samples by conventional PCR and sequencing. A quantitative PCR method was developed to monitor and finally verify successful treatment. This novel approach to monitoring mycoplasma urinary tract infections is conceptually simple, and provides rapid results. It may have wider application in monitoring treatment efficacy for infections with other Mycoplasma spp. as well as additional organisms that are difficult to culture. SIGNIFICANCE AND IMPACT OF THE STUDY: In this study, we highlight two different findings, detection of Ureaplasma canigenitalium in a dog with chronic urinary tract infection and development of a quantitative real-time PCR test to track treatment results in an infected dog. This report is the first report of detection of U. canigenitalium in one dog in Australia. This novel qPCR method for monitoring mycoplasma urinary tract infections is conceptually simple and provides results fast. It will have wider applications in monitoring treatment efficacy for infections with mycoplasmas and mycoplasma-like organisms that are difficult to culture, and provides a sensitive guide to treatment progress.

VetCompass Australia is veterinary medical records-based research coordinated with the global VetCompass endeavor to maximize its quality and effectiveness for Australian companion animals (cats, dogs, and horses). Bringing together all seven Australian veterinary schools, it is the first nationwide surveillance system collating clinical records on companion-animal diseases and treatments. VetCompass data service collects and aggregates real-time, clinical records for researchers to interrogate, delivering sustainable and cost-effective access to data from hundreds of veterinary practitioners nationwide. Analysis of these clinical records will reveal geographical and temporal trends in the prevalence of inherited and acquired diseases, identify frequently prescribed treatments, revolutionize clinical auditing, help the veterinary profession to rank research priorities, and assure evidence-based companion-animal curricula in veterinary schools. VetCompass Australia will progress in three phases: (1) roll-out of the VetCompass platform to harvest Australian veterinary clinical record data; (2) development and enrichment of the coding (data-presentation) platform; and (3) creation of a world-first, real-time surveillance interface with natural language processing (NLP) technology. The first of these three phases is described in the current article. Advances in the collection and sharing of records from numerous practices will enable veterinary professionals to deliver a vastly improved level of care for companion animals that will improve their quality of life.

OBJECTIVE:To measure the prevalence of internal tandem duplications (ITDs) in exon 11 of the proto-oncogene C-KIT in a sample of Australian cutaneous canine mast cell tumours (MCTs) drawn from general practice and to evaluate relationships between tumour mutation status and prognostic factors including signalment, tumour histological grade, tumour anatomical location and tumour size.METHODS:C-KIT exon 11 ITDs were detected by PCR in DNA extracted from formalin-fixed, paraffin-embedded canine MCTs sourced from three veterinary diagnostic laboratories in Adelaide and Melbourne. Tumours were graded according to two different systems (Patnaik and Kiupel systems) by board-certified anatomical pathologists blinded to the PCR results. Relationships between tumour mutation status and prognostic factors were evaluated using a generalised binary logistic regression analysis.RESULTS:ITDs were identified in 13 of 74 cutaneous canine MCT samples, giving an overall prevalence of 17.6% (95% confidence interval: 8.9-26.2%). ITDs were detected in 10 of 18 Patnaik grade III MCTs (55.6%) and 11 of 22 Kiupel high-grade MCTs (50%). Wald chi-square analysis revealed that detection of tumour ITDs was significantly associated with both Patnaik's and Kiupel's histologic grading systems (each: P < 0.001). The presence of the ITDs in MCTs was not associated with signalment, tumour anatomical location or tumour size.CONCLUSION:The prevalence of C-KIT exon 11 ITDs in Australian canine MCTs is similar to the prevalence in overseas canine populations (overall prevalence in Australia approximately 18%). ITDs were more frequently identified in higher grade MCTs.

Vaccination is becoming a more acceptable option in the effort to eradicate avian influenza viruses (AIV) from commercial poultry, especially in countries where AIV is endemic. The main concern surrounding this option has been the inability of the conventional serological tests to differentiate antibodies produced due to vaccination from antibodies produced in response to virus infection. In attempts to address this issue, at least six strategies have been formulated, aiming to differentiate infected from vaccinated animals (DIVA), namely (i) sentinel birds, (ii) subunit vaccine, (iii) heterologous neuraminidase (NA), (iv) nonstructural 1 (NS1) protein, (v) matrix 2 ectodomain (M2e) protein, and (vi) haemagglutinin subunit 2 (HA2) glycoprotein. This short review briefly discusses the strengths and limitations of these DIVA strategies, together with the feasibility and practicality of the options as a part of the surveillance program directed toward the eventual eradication of AIV from poultry in countries where highly pathogenic avian influenza is endemic.