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A 2‐year‐old male desexed Ragdoll cat with a 1‐year history of sneezing and nasal discharge presented with a large subcutaneous cervical mass, identified as the right medial retropharyngeal lymph node on computed tomography (CT). A right orbital mass, destructive sino‐nasal cavity disease and multiple pulmonary nodules were also identified. Aspergillus felis was cultured from the lymph node. After treatment with posaconazole and liposomal amphotericin B the lymph node enlargement and orbital mass resolved but left frontal sinus involvement and pulmonary lesions persisted despite additional caspofungin therapy. The cat was euthanized 14 months after diagnosis with dysphagia and chronic progressive exophthalmos. A meningeal granuloma with intravascular fungal hyphae was identified at post‐mortem and A felis was cultured from the left frontal sinus and a right retrobulbar fungal granuloma. This case demonstrates that disseminated disease is a possible sequel to invasive fungal rhinosinusitis caused by A felis in cats.

Cryptic species in Aspergillus section Fumigati are increasingly reported to cause invasive aspergillosis in humans and animals. These infections are often refractory to treatment because of intrinsic antifungal resistance. We report two cases of invasive fungal rhinosinusitis in domestic cats caused by A. udagawae and A. felis. Clinical signs resolved after combined therapy including posaconazole, caspofungin and terbinafine. Both cases remained asymptomatic more than 2 years from initial presentation.

Azole-resistant environmental Aspergillus fumigatus presents a threat to public health but the extent of this threat in Southeast Asia is poorly described. We conducted environmental surveillance in the Mekong Delta region of Vietnam, collecting air and ground samples across key land-use types, and determined antifungal susceptibilities of Aspergillus section Fumigati (ASF) isolates and azole concentrations in soils. Of 119 ASF isolates, 55% were resistant (or non-wild type) to itraconazole, 65% to posaconazole and 50% to voriconazole. Azole resistance was more frequent in A. fumigatus sensu stricto isolates (95%) than other ASF species (32%). Resistant isolates and agricultural azole residues were overrepresented in samples from cultivated land. cyp51A gene sequence analysis showed 38/56 resistant A. fumigatus sensu stricto isolates carried known resistance mutations, with TR34 /L98H most frequent (34/38).

We tested 50 cats from coronavirus disease households or close contacts in Hong Kong, China, for severe acute respiratory syndrome coronavirus 2 RNA in respiratory and fecal samples. We found 6 cases of apparent human-to-feline transmission involving healthy cats. Virus genomes sequenced from 1 cat and its owner were identical.

A nine-year-old domestic short hair cat was presented for a nasal planum mass, nasal discharge, hyporexia and weight loss. On physical examination nasal proliferative and ulcerative lesions and submandibular lymphadenopathy were identified. Cytology, histopathology, fungal culture, antigen serology and MALDI-TOF confirmed cryptococcal rhinitis with regional mandibular lymph node involvement due to Cryptococcus neoformans infection. This is the first reported case of cryptococcosis in a feline patient in Hong Kong.

Canine parvovirus (CPV) is a major enteric pathogen of dogs worldwide that emerged in the late 1970s from a feline parvovirus (FPV)-like ancestral virus. Shortly after its emergence, variant CPVs acquired amino acid (aa) mutations in key capsid residues, associated with biological and/or antigenic changes. This study aimed to identify and analyse CPV variants and their capsid mutations amongst Australian dogs, to gain insights into the evolution of CPV in Australia and to investigate relationships between the disease and vaccination status of dogs from which viruses were detected. CPV VP2 sequences were amplified from 79 faecal samples collected from dogs with parvoviral enteritis at 20 veterinary practices in five Australian states. The median age at diagnosis was 4 months (range 1-96 months). Only 3.7% of dogs with vaccination histories had completed recommended vaccination schedules, while 49% were incompletely vaccinated and 47.2% were unvaccinated. For the first time, CPV-2b has emerged as the dominant antigenic CPV variant circulating in dogs with parvoviral enteritis in Australia, comprising 54.4% of viruses, while CPV-2a and CPV-2 comprised 43.1% and 2.5%, respectively. The antigenic variant CPV-2c was not identified. Analysis of translated VP2 sequences revealed a vast repertoire of amino acid (aa) mutations. Several Australian CPV strains displayed signatures in the VP2 protein typical of Asian CPVs, suggesting possible introduction of CPV strains from Asia, and/or CPV circulation between Asia and Australia. Canine parvoviruses were identified containing aa residues typical of FPV at key capsid (VP2) positions, representing reverse mutations or residual mutations retained from CPV-2 during adaptation from an FPV-like ancestor, suggesting that evolutionary intermediates between CPV-2 and FPV are circulating in the field. Similarly, intermediates between CPV-2a-like viruses and CPV-2 were also identified. These findings help inform a better understanding of the evolution of CPV in dogs.

Ongoing surveillance of Toxoplasma gondii seroprevalence and exposure risks in owned cats is important to identify effective mechanisms to decrease the prevalence of this global zoonotic parasite. We aimed to determine the seroprevalence of T. gondii and risk factors for seropositivity in owned domestic cats in Australia. Sera, signalment data, postcode, and completed owner-questionnaires surveying diet composition and lifestyle factors were collected for cats presenting to 18 veterinary clinics across Australia. T. gondii-specific IgG was measured by enzyme-linked immunosorbent assay. Data were analyzed using univariable and multivariable logistic regression to evaluate risk factors associated with positive T. gondii IgG serology. Among 417 cats, T. gondii seroprevalence was 39%. More than two-thirds of cats tested (69%) had outdoor access and 59% were fed a diet containing raw meat. Univariable analyses identified, age (>1 year, p 1 year, odds ratio [OR]: 7.15) and feeding of raw meat (OR: 2.23) remained significant risk factors (p

A six-year-old domestic shorthair cat was presented for a subcutaneous digital nodular lesion on the right forelimb. On physical examination a similar lesion was identified on the right hindlimb. Disseminated cutaneous phaeohyphomycosis was diagnosed from histopathological changes in representative tissue biopsies and fungal culture. The isolate was identified by sequencing of ITS rDNA as Exophiala spinifera. This is the first report of disseminated cutaneous disease caused by E. spinifera in the cat. Keywords: Black yeasts, Exophiala, Phaehyphomycosis, Histopathology, Molecular diagnosis

Fungal rhinosinusitis, including sinonasal aspergillosis (SNA) and sino-orbital aspergillosis (SOA), is the most common type of aspergillosis encountered in cats. Other focal forms of aspergillosis including disseminated invasive aspergillosis occur less frequently. SOA is an invasive mycosis that is increasingly recognized and is most commonly caused by Aspergillus felis, a close relative of Aspergillus fumigatus. SNA can be invasive or noninvasive and is most commonly caused by A fumigatus and Aspergillus niger. Molecular methods are required to correctly identify the fungi that cause SNA and SOA. SNA has a favorable prognosis with treatment, whereas the prognosis for SOA remains poor.

Recent advances in molecular genetics have enabled a great deal of information about species to be obtained from analysis of non-invasively collected samples such as scat. Scat provides genetic information via residual host DNA on the outside of the scat, via characterising the genetic makeup of intestinal microbes that are present in the scat, or by examining the DNA remnants of prey items that have passed through the animal’s digestive tract. In this review, we provide a case study to demonstrate how these approaches are being used to better understand the threatened Tasmanian devil in the landscape, and to support the species’ conservation. Scat analysis enables us to quantify the genetic diversity of remote populations, where trapping is logistically challenging. We are beginning to learn how conservation management impacts the microbiome of threatened species, and investigate how various management strategies may be impacting the diverse array of bacteria and viruses that devils, like all animal species, are host to. We are using scat samples to better understand the interaction between devils and other animals in their environment by learning more about what they eat. We explore the strengths and challenges of these approaches by comparing our work to that conducted in other species. Finally, we provide specific examples of how our results are being integrated into conservation strategy for the devil.

Feline calicivirus (FCV) causes upper respiratory tract disease (URTD) and sporadic outbreaks of virulent systemic disease (FCV-VSD). The basis for the increased pathogenicity of FCV-VSD viruses is incompletely understood, and antivirals for FCV-VSD have yet to be developed. We investigated the clinicoepidemiology and viral features of three FCV-VSD outbreaks in Australia and evaluated the in vitro efficacy of nitazoxanide (NTZ), 2′-C-methylcytidine (2CMC) and NITD-008 against FCV-VSD viruses. Overall mortality among 23 cases of FCV-VSD was 39%. Metagenomic sequencing identified five genetically distinct FCV lineages within the three outbreaks, all seemingly evolving in situ in Australia. Notably, no mutations that clearly distinguished FCV-URTD from FCV-VSD phenotypes were identified. One FCV-URTD strain likely originated from a recombination event. Analysis of seven amino-acid residues from the hypervariable E region of the capsid in the cultured viruses did not support the contention that properties of these residues can reliably differentiate between the two pathotypes. On plaque reduction assays, dose–response inhibition of FCV-VSD was obtained with all antivirals at low micromolar concentrations, NTZ EC50, 0.4–0.6 µM, TI = 21, 2CMC EC50, 2.7–5.3 µM, TI &gt, 18, NITD-008, 0.5 to 0.9 µM, TI &gt, 111. Investigation of these antivirals for the treatment of FCV-VSD is warranted.

Although feline urinary tract diseases cause high morbidity and mortality rates, and subclinical bacteriuria is not uncommon, the feline urinary microbiome has not been characterized. We conducted a case-control study to identify the feline urinary bladder microbiome and assess its association with chronic kidney disease (CKD), feline idiopathic cystitis (FIC), and positive urine cultures (PUCs). Of 108 feline urine samples subjected to 16S rRNA gene sequencing, 48 (44.4%) samples reached the 500-sequence rarefaction threshold and were selected for further analysis, suggesting that the feline bladder microbiome is typically sparse. Selected samples included 17 CKD, 9 FIC, 8 PUC cases and 14 controls. Among these, 19 phyla, 145 families, and 218 genera were identified. Proteobacteria were the most abundant, followed by Firmicutes. Notably, four major urotypes were identified, including two urotypes predominated by Escherichia-Shigella or Enterococcus and two others characterized by relatively high alpha diversity, Diverse 1 and Diverse 2. Urotype was associated with disease status (P value of 0.040), with the Escherichia-Shigella-predominant urotype being present in 53% of CKD cases and in all of the Escherichia coli PUC cases. Reflecting these patterns, the overall microbial composition of CKD cases was more similar to that of E. coli PUC cases than to that of controls (P value of

Feline panleukopenia (FPL) is caused by a Carnivore protoparvovirus infection. Feline parvovirus (FPV) causes most cases. When Canine parvovirus 2 (CPV-2) first emerged, it could not replicate in cats. All current CPV variants (CPV-2a-c) can infect cats to cause subclinical disease or FPL. Feline panleukopenia has re-emerged in Australia in shelter cats associated with failure to vaccinate. Parvoviruses can remain latent in mononuclear cells post-infection. Molecular methods such as polymerase chain reaction are used to determine the infecting strain. Current perspectives on causes, epidemiology, diagnosis, treatment, prognostic indicators, and management of outbreaks in shelters are reviewed.

SARS-CoV-2 emerged from animals and is now easily transmitted between people. Sporadic detection of natural cases in animals alongside successful experimental infections of pets, such as cats, ferrets and dogs, raises questions about the susceptibility of animals under natural conditions of pet ownership. Here, we report a large-scale study to assess SARS-CoV-2 infection in 919 companion animals living in northern Italy, sampled at a time of frequent human infection. No animals tested PCR positive. However, 3.3% of dogs and 5.8% of cats had measurable SARS-CoV-2 neutralizing antibody titers, with dogs from COVID-19 positive households being significantly more likely to test positive than those from COVID-19 negative households. Understanding risk factors associated with this and their potential to infect other species requires urgent investigation., SARS-CoV-2 can infect cats and dogs, but the extent to which pets are infected in households remains unclear. Here, Patterson et al. test 919 companion animals in northern Italy and find that some dogs and cats from COVID-19 positive households can test positive for COVID-19 neutralizing antibodies, with dogs significantly more likely to do so if they came from COVID-19 positive households.

Hepatitis B virus (HBV) is a major cause of liver disease in humans including chronic hepatitis and hepatocellular carcinoma. Domestic cat hepadnavirus (DCH), a novel HBV-like hepadnavirus, was identified in domestic cats in 2018. From 6.5 %-10.8 % of pet cats are viremic for DCH and altered serological markers suggestive of liver damage have been identified in 50 % of DCH-infected cats. DCH DNA has been detected in association with characteristic lesions of chronic hepatitis and with hepatocellular carcinoma in cats, suggesting a possible association. In this study longitudinal molecular screening of cats infected with DCH was performed to determine if DCH can cause chronic infections in cats. Upon re-testing of sera from five DCH-positive animals, 2-10 months after the initial diagnosis, three cats tested negative for DCH on two consecutive occasions using quantitative PCR. Two other cats remained DCH-positive, including an 8-month-old female cat re-tested four months after the initial positive result, and a 9-year-old male cat, which tested positive for DCH on six occasions over an 11-month period. The latter had a history of chronic hepatopathy with jaundice, lethargy and elevated serum alanine transaminase levels (ALT). During the period of observation, DCH titers ranged between 1.64 × 105 and 2.09 × 106 DNA copies/mL and ALT was persistently elevated, suggesting chronic infection. DCH DNA was not detected in oral, conjunctival, preputial and rectal swabs from the two animals collected at several time points. Long-term (chronic) infection would be consistent with the relatively high number of viremic cats identified in epidemiological investigations, with the possible association of DCH with chronic hepatic pathologies and with what described with HBV in human patients.

Astroviruses, isolated from numerous avian and mammalian species including humans, are commonly associated with enteritis and encephalitis. Two astroviruses have previously been identified in cats, and while definitive evidence is lacking, an association with enteritis is suggested. Using metagenomic next-generation sequencing of viral nucleic acids from faecal samples, we identified two novel feline astroviruses termed Feline astrovirus 3 and 4. These viruses were isolated from healthy shelter-housed kittens (Feline astrovirus 3, 6448 bp) and from a kitten with diarrhoea that was co-infected with Feline parvovirus (Feline astrovirus 4, 6549 bp). Both novel astroviruses shared a genome arrangement of three open reading frames (ORFs) comparable to that of other astroviruses. Phylogenetic analysis of the concatenated ORFs, ORF1a, ORF1b and capsid protein revealed that both viruses were phylogenetically distinct from other feline astroviruses, although their precise evolutionary history could not be accurately determined due to a lack of resolution at key nodes. Large-scale molecular surveillance studies of healthy and diseased cats are needed to determine the pathogenicity of feline astroviruses as single virus infections or in co-infections with other enteric viruses.

The burden of aspergillosis, especially Chronic Pulmonary Aspergillosis, is increasingly recognized, and the increasing presence of azole-resistant environmental Aspergillus fumigatus has been highlighted as a health risk. However, a sizable minority of aspergillosis is caused by Aspergillus flavus, which is assumed to be sensitive to azoles but is infrequently included in surveillance. We conducted environmental sampling at 150 locations in a rural province of southern Vietnam. A. flavus isolates were identified morphologically, their identity was confirmed by sequencing of the beta-tubulin gene, and then they were tested for susceptibility to azoles and amphotericin B according to EUCAST methodologies. We found that over 85% of A. flavus isolates were resistant to at least one azole, and half of them were resistant to itraconazole. This unexpectedly high prevalence of resistance demands further investigation to determine whether it is linked to agricultural azole use, as has been described for A. fumigatus. Clinical correlation is required, so that guidelines can be adjusted to take this information into account.

Surrogate neutralization assays for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that can be done without biosafety level 3 containment and in multiple species are desirable. We evaluate a recently developed surrogate virus neutralization test (sVNT) in comparison to 90% plaque reduction neutralization tests (PRNT90) in human, canine, cat, and hamster sera. With PRNT90 as the reference, sVNT had sensitivity of 98.9% and specificity of 98.8%. Using a panel of immune sera corresponding to other coronaviruses, we confirm the lack of cross-reactivity to other coronaviruses in SARS-CoV-2 sVNT and PRNT90, except for cross-reactivity to SARS-CoV-1 in sVNT.

Objectives To describe the clinicopathological findings and outcomes of cases of feline congenital hypothyroidism diagnosed in a single veterinary hospital in Santiago, Chile. Materials and methods Medical records were searched for cases of congenital hypothyroidism over an 18-month period. Inclusion criteria were a diagnosis of congenital hypothyroidism based on consistent historical and clinical findings, a low or low-normal serum total T4 and elevated serum canine TSH (cTSH). Results Six unrelated cats ranging in age from 4 to 19 months met the inclusion criteria. The most common historical signs were small stature and lethargy. All cats had disproportionate dwarfism, delayed tooth eruption, retained deciduous teeth, bilateral palpable goitres and low rectal temperatures. Other findings were bradycardia, obesity, poor hair coat and focal alopecia on the ventral aspects of the elbows and hocks. In all cases, cTSH was markedly elevated. Sequential changes noted after the initiation of therapy included normal T4 after 6 weeks, improved hair coat and increased physical activity by 8 weeks, normal cTSH by 10 weeks and normal physical appearance and dentition after 4 months. Goitres shrank markedly but remained palpable. Hypothyroidism was well managed clinically in all cases 2 years after diagnosis except for one cat that died of unrelated causes. Clinical significance This is the first report to describe a cluster of congenital hypothyroidism cases in non-related cats that were presented over a short period of time. Growth defects resolve with treatment, even in cats diagnosed after puberty. Larger, prospective multi-centre studies are warranted to determine the incidence of congenital hypothyroidism in cats.

Highlights • Despite extensive vaccination, canine parvovirus (CPV) still represents one of the major causes of pups’ mortality. • CPV immunisation failures occur frequently and recognize different reasons. • Interference by maternally-derived antibodies is the main cause of CPV immunisation failures. • Eradication of CPV infection is a challenge for the future, but it will not be achieved in a short time, Despite extensive vaccination, canine parvovirus (CPV) remains a leading infectious cause of canine mortality, especially among juveniles. This review provides an update on CPV vaccine types and vaccination protocols. The design of CPV prevention strategies and vaccination programs with a goal of herd immunity has been hampered by deficiencies of studies that model companion animal viral infections and inform an understanding of the basic reproduction number. However, the most important issue in eradication of CPV disease is represented by immunisation failures including: i) the presence of interfering titres of maternally-derived antibodies; ii) the presence of non-responders; and iii) possible reversion to virulence. In contrast, the role of the CPV variants in immunisation failures is widely debated. Taking into account the reduced circulation of canine distemper virus and canine adenovirus type 1 in countries where extensive vaccination is carried out, more effort should be made to aim for CPV eradication, including antibody testing to determine the optimal time for vaccinations of pups and adults and homogeneous vaccine coverage of dog population.

Canine parvovirus (CPV) is a cause of severe disease in dogs globally, yet is preventable by vaccination. A range of vaccination protocols are used by veterinary practitioners with evidence suggesting some protocols provide better protection than others in high infection-risk situations. This study investigated associations between veterinarians' vaccination recommendations and hospital remoteness, socioeconomic disadvantage, CPV caseload, and veterinarian perceptions and demographics. A national Australian veterinary survey in 2017 received 569 practitioner responses from 534 unique hospitals (23.6 % response rate). Respondents from major city hospitals had the lowest perceptions of the national CPV caseload (p0.0001). Those from hospitals with mild to moderate caseloads (6-40 cases per annum) recommended more frequent puppy revaccination - which is considered more protective - than those with the highest caseload (p = 0.0098), which might increase vaccination failure risk. Respondents from the most socioeconomically disadvantaged regions were over-represented in recommending annual revaccination of adult dogs; those from the least disadvantaged regions were over-represented in recommending triennial revaccination (p0.0001). Hospitals with higher CPV caseloads, greater socioeconomic disadvantage or increased remoteness did not favor two puppy vaccination protocols that are considered more protective (younger first vaccination age or older final vaccination age), despite these regions presenting higher CPV caseload risk. Titer testing to determine whether to revaccinate was more likely to be used in major city hospitals (p = 0.0052) and less disadvantaged areas (p = 0.0550). University of graduation was associated with CPV caseload, remoteness and level of socioeconomic disadvantage of the region where the graduate worked. University of graduation was significantly associated with age for final puppy vaccination and titer-testing recommendations. Graduates from one university were over-represented in recommending an earlier (10-week) finish protocol and titer testing, compared to all other universities. Year and university of graduation, and respondent's age were associated with a number of vaccination protocol recommendations suggesting that inherent biases might affect veterinarians' decisions. Emphasis on currently recommended vaccination protocols in undergraduate curricula and more protective vaccination protocol use in higher-risk regions could reduce immunization failure and CPV caseload.

Canine parvovirus (CPV) has been reported throughout the world since the late 1970s. Published information was reviewed to draw insights into the epidemiology, pathogenesis, diagnosis, treatment and outcomes of CPV disease in Australia and the role of scientific research on CPV occurrence, with key research discoveries and knowledge gaps identified. Australian researchers contributed substantially to early findings, including the first reported cases of parvoviral myocarditis, investigations into disease aetiopathogenesis, host and environmental risk factors and links between CPV and feline panleukopenia. Two of the world's first CPV serological surveys were conducted in Australia and a 1980 national veterinary survey of Australian and New Zealand dogs revealed 6824 suspected CPV cases and 1058 deaths. In 2010, an Australian national disease surveillance system was launched; 4940 CPV cases were reported between 2009 and 2014, although underreporting was likely. A 2017 study estimated national incidence to be 4.12 cases per 1000 dogs, and an annual case load of 20,110 based on 4219 CPV case reports in a survey of all Australian veterinary clinics, with a 23.5% response rate. CPV disease risk factors identified included socioeconomic disadvantage, geographical location (rural/remote), season (summer) and rainfall (recent rain and longer dry periods both increasing risk). Age

Multiple, epizootic outbreaks of feline panleukopenia (FPL) caused by feline parvovirus(FPV) occurred in eastern Australia between 2014 and 2018. Most affected cats were unvaccinated.We hypothesised that low population immunity was a major driver of re‐emergent FPL. The aim ofthis study was to (i) determine the prevalence and predictors of seroprotective titres to FPV amongshelter‐housed and owned cats, and (ii) compare the prevalence of seroprotection between a regionaffected and unaffected by FPL outbreaks. FPV antibodies were detected by haemagglutinationinhibition assay on sera from 523 cats and titres &ge, 1:40 were considered protective. Socioeconomicindices based on postcode and census data were included in the risk factor analysis. The prevalenceof protective FPV antibody titres was high overall (94.3%), even though only 42% of cats wereknown to be vaccinated, and was not significantly different between outbreak and non‐outbreakregions. On multivariable logistic regression analysis vaccinated cats were 29.94 times more likelyto have protective FPV titres than cats not known to be vaccinated. Cats from postcodes of relativelyless socioeconomic disadvantage were 5.93 times more likely to have protective FPV titres. Thepredictors identified for FPV seroprotective titres indicate targeted vaccination strategies in regionsof socioeconomic disadvantage would be beneficial to increase population immunity. The criticallevel of vaccine coverage required to halt FPV transmission and prevent FPL outbreaks should bedetermined.

Background: Azole-resistant Aspergillus fumigatus (ARAF) presents a threat to global public health, particularly where prior tuberculosis or underlying lung disease is prevalent. Southeast Asia is estimated to have a large burden of Aspergillus disease yet mycology diagnostic laboratory capacity is limited and systematic surveillance for drug resistance is absent. ARAF’s threat is thus poorly understood in this populous region. Methods: We conducted environmental surveillance in southern Vietnam, collecting air and ground samples across land-use types including cultivated land, urban residential land, and national park. We determined susceptibilities of A. fumigatus and non-fumigatus Aspergillus section Fumigati (ASF) isolates using EUCAST methodology, and measured residual agricultural azole concentrations in soil using liquid chromatography / tandem mass spectrometry. Findings: 95·2% of A. fumigatus isolates (59/62) were azole-resistant (31·6% for non- fumigatus ASF isolates (18/57)). Of all 119 ASF isolates, 55% were resistant or non-wild type to itraconazole, 65% to posaconazole and 50% to voriconazole. Both resistant isolates and agricultural azole residues were over-represented in cultivated land. The odds ratio for azole-resistance being detected, compared to national park sites, was ranged from 3·15-7·16 in cultivated lands types, and was highest in urban residential sites (9·31, p=0.0002). cyp51A gene sequence analysis showed 38/56 resistant A. fumigatus isolates carried known resistance mutations, with TR34/L98H most frequent (34/38). Interpretation: Our data demonstrate alarmingly high levels of azole-resistant A. fumigatus in this region, which challenge the reliance of existing treatment guidelines on empiric azole therapy. Funding Statement: This project received internal funding from the University of Sydney. Declaration of Interests: None of the authors have any financial and personal potential conflicts of interest. Ethics Approval Statement: National Lung Hospital, Hanoi, Vietnam provided ethical approval for the study.

Feline calicivirus (FCV) is a major pathogen of cats associated with either respiratory disease or systemic disease, but its possible role as an enteric pathogen is neglected. Using RT-PCR, the RNA of FCV was identified in 25.9% (62/239) of stools of cats with enteritis and in 0/58 (0%) of cats without diarrhoea or other clinical signs. Isolates of enteric origin were obtained and a large 3.2-kb portion of the genome was sequenced, encompassing the 3' end of the RNA polymerase, the capsid protein precursor and the minor capsid protein. Also, the complete genome sequence of one such strain, the 160/2015/ITA, was determined. Upon sequence analysis, the enteric viruses were found to be genetically heterogeneous and to differ from each other and from isolates of respiratory origin. The enteric isolates were found to be more resistant to low pH conditions, to trypsin and to bile treatment than respiratory isolates. Overall, these findings are consistent with the hypothesis that some FCVs may acquire enteric tropism and eventually act as enteric pathogens. Whether this enteric tropism is maintained stably and whether it may affect, to some extent, the ability of the virus to trigger the classical and/or hypervirulent forms of disease should be assessed. Also, FCV should be included in the diagnostic algorithms of enteric diseases of cats to gain further information about FCV strains displaying enteric pathotype.

Highlights • 11 % of Australian veterinary hospitals reported >40 canine parvovirus cases in 2016. • Socioeconomic disadvantage was the strongest risk factor for canine parvovirus. • Euthanasia is the leading cause of fatality for canine parvovirus related disease. • Hottest month of the year is associated with canine parvovirus case occurrence. • Low rainfall is associated with higher canine parvovirus cases., Infection of canids with canine parvovirus (CPV) can result in severe, often fatal disease. This study aimed to examine climatic, socioeconomic and geographic risk factors for CPV infection and CPV-associated euthanasia in Australia. Australian veterinary hospital responses (534; 23.5 %) to a national veterinary survey of CPV case occurrences and euthanasias in 2016 were used. Severe caseloads (>40 cases per annum) were reported by 26 (11 %) hospitals (median 60 cases; IQR 50–110). Case reporting, case numbers, and without-treatment euthanasia were significantly associated with disadvantage across all Socio-Economic Index for Areas quintiles (p

Objectives The aim of this study was to conduct a comprehensive assessment of feline infectious upper respiratory tract infection (URTI) and disease (URTD) in Australian cats. Methods Laboratory data demonstrating URTI from feline URTD multiplex PCR panel (feline herpesvirus 1 [FHV-1], feline calicivirus [FCV], Bordetella bronchiseptica, Chlamydophila felis, Mycoplasma felis and H1N1 influenza) submissions in Australia (2013–2015) were obtained. For comparison, reports of feline URTD during the same time period were sourced from a voluntary companion animal disease surveillance system. Results A total of 3126 samples were submitted for testing; 1533 (49%) were positive. Of these, the most commonly detected agents were M felis (21.5%) and FCV (16.0%) alone, followed by FCV and M felis (13.4%) together as a respiratory infection complex, then FHV-1 (7.0%) alone. During the study period, there were 262 reports of 320 clinical feline URTD cases. Most cases (69%) were reported from New South Wales, Conclusions and relevance Feline URTI and URTD cause substantial impact in Australia, being most commonly associated with M felis and FCV infection. This information can be used by veterinarians to educate clients about prevention and management of this important infectious disease of cats.

Canine parvovirus (CPV) and feline panleukopenia virus (FPV) are deoxyriboncucleic acid (DNA) viruses in the taxon Carnivore protoparvovirus 1. Exposure of cats to either CPV or FPV results in productive infection and faecal shedding of virus. Asymptomatic shedding of CPVs by one-third of shelter-housed cats in a UK study suggests that cats may be an important reservoir for parvoviral disease in dogs. The aim of this cross-sectional study was to determine the prevalence of faecal shedding of CPVs in asymptomatic shelter-housed cats in Australia. Faecal samples (n=218) were collected from cats housed in three shelters receiving both cats and dogs, in Queensland and NSW. Molecular testing for Carnivore protoparvovirus 1 DNA was performed by polymerase chain reaction (PCR) amplification followed by DNA sequencing of the VP2 region to differentiate CPV from FPV. Carnivore protoparvovirus 1 DNA was detected in only four (1.8%, 95% confidence interval 0.49-4.53%) faecal samples from a single shelter. Sequencing identified all four positive samples as FPV. Faecal shedding of CPV by shelter-cats was not detected in this study. While the potential for cross-species transmission of CPV between cats and dogs is high, this study found no evidence of a role for cats in maintaining CPV in cat and dog populations through faecal shedding in the regions tested.

Papillomaviruses infect the skin and mucosal surfaces of diverse animal hosts with consequences ranging from asymptomatic colonization to highly malignant epithelial cancers. Increasing evidence suggests a role for papillomaviruses in the most common cutaneous malignancy of domestic cats, squamous cell carcinoma (SCC). Using total DNA sequencing we identified a novel feline papillomavirus in a nasal biopsy taken from a cat presenting with both nasal cavity lymphoma and recurrent squamous cell carcinoma affecting the nasal planum. We designate this novel virus as Felis catus papillomavirus 6 (FcaPV6). The complete FcaPV6 7453 bp genome was similar to those of other feline papillomaviruses and phylogenetic analysis revealed that it was most closely related to FcaPV3, although was distinct enough to represent a new viral species within the genus Taupapillomavirus. Archived excisional biopsy of the SCC, taken 20 months prior to presentation, was intensely positive on p16 immunostaining. FcaPV6, amplified using virus-specific, but not consensus, PCR was the only papillomavirus detected in DNA extracted from the SCC. Conversely, renal lymphoma, sampled at necropsy two months after presentation, tested negative on FcaPV6-specific PCR. In sum, using metagenomics we demonstrate the presence of a novel feline papillomavirus in association with cutaneous squamous cell carcinoma.

Feline panleukopenia (FPL), a frequently fatal disease of cats, is caused by feline parvovirus (FPV) or canine parvovirus (CPV). We investigated simultaneous outbreaks of FPL between 2014 and 2018 in Australia, New Zealand and the United Arab Emirates (UAE) where FPL outbreaks had not been reported for several decades. Case data from 989 cats and clinical samples from additional 113 cats were obtained to determine the cause of the outbreaks and epidemiological factors involved. Most cats with FPL were shelter-housed, 9 to 10 weeks old at diagnosis, unvaccinated, had not completed a primary vaccination series or had received vaccinations noncompliant with current guidelines. Analysis of parvoviral VP2 sequence data confirmed that all FPL cases were caused by FPV and not CPV. Phylogenetic analysis revealed that each of these outbreaks was caused by a distinct FPV, with two virus lineages present in eastern Australia and virus movement between different geographical locations. Viruses from the UAE outbreak formed a lineage of unknown origin. FPV vaccine virus was detected in the New Zealand cases, highlighting the difficulty of distinguishing the co-incidental shedding of vaccine virus in vaccinated cats. Inadequate vaccination coverage in shelter-housed cats was a common factor in all outbreaks, likely precipitating the multiple re-emergence of infection events.

Background The prevalence of azole resistance in Aspergillus fumigatus is uncertain in Australia. Azole exposure may select for resistance. We investigated the frequency of azole resistance in a large number of clinical and environmental isolates. Methods A. fumigatus isolates [148 human, 21 animal and 185 environmental strains from air (n = 6) and azole-exposed (n = 64) or azole-naive (n = 115) environments] were screened for azole resistance using the VIPcheck™ system. MICs were determined using the Sensititre™ YeastOne YO10 assay. Sequencing of the Aspergillus cyp51A gene and promoter region was performed for azole-resistant isolates, and cyp51A homology protein modelling undertaken. Results Non-WT MICs/MICs at the epidemiological cut-off value of one or more azoles were observed for 3/148 (2%) human isolates but not amongst animal, or environmental, isolates. All three isolates grew on at least one azole-supplemented well based on VIPcheck™ screening. For isolates 9 and 32, the itraconazole and posaconazole MICs were 1 mg/L (voriconazole MICs 0.12 mg/L); isolate 129 had itraconazole, posaconazole and voriconazole MICs of >16, 1 and 8 mg/L, respectively. Soil isolates from azole-exposed and azole-naive environments had similar geometric mean MICs of itraconazole, posaconazole and voriconazole (P > 0.05). A G54R mutation was identified in the isolates exhibiting itraconazole and posaconazole resistance, and the TR34/L98H mutation in the pan-azole-resistant isolate. cyp51A modelling predicted that the G54R mutation would prevent binding of itraconazole and posaconazole to the haem complex. Conclusions Azole resistance is uncommon in Australian clinical and environmental A. fumigatus isolates; further surveillance is indicated.

Whether subclinical shedding of canine parvovirus (CPV) by cats might contribute to the epidemiology of canine CPV infections, particularly in facilities housing both cats and dogs, requires clarification. Conflicting results are reported to date. Using conventional PCR (cPCR) to amplify the VP2 gene, shedding of the CPV variants (CPV-2a, 2b, 2c) by healthy cats in multi-cat environments was reportedly common in Europe but rare in Australia. The aim of this study was to determine whether low-level faecal CPV shedding occurs in multi-cat environments in Australia and Italy using a TaqMan real-time PCR to detect Carnivore protoparvovirus 1 (CPV and feline parvovirus, FPV) DNA, and minor-groove binder probe real-time PCR assay to differentiate FPV and CPV types and to characterize CPV variants. In total, 741 non-diarrhoeic faecal samples from shelters in Australia (n = 263) and from shelters or cat colonies in Italy (n = 478) were tested. Overall, Carnivore protoparvovirus 1 DNA was detected in 49 of 741 (6.61 %) samples. Differentiation was possible for 31 positive samples. FPV was most common among positive samples (28/31, 90.3 %). CPV was detected in 4/31 samples (12.9 %) including CPV-2a in one sample, CPV-2b in another and co-infections of FPV/CPV-2b and CPV-2a/CPV-2b in the remaining two samples. A high rate of subclinical FPV infection was detected in one shelter during an outbreak of feline panleukopenia, during which 21 of 22 asymptomatic cats (95.5 %) sampled were shedding FPV. Faecal shedding of CPV by cats in multi-cat environments is uncommon suggesting that domestic cats are not significant reservoirs of CPV.

Canine parvovirus type 2 (CPV-2) infection is associated with severe gastroenteritis in puppies. Quantification of CPV-2 specific antibodies before vaccination can reveal the presence of interfering maternal-derived immunity and facilitate timing of effective immunisation. Inhibition of haemagglutination (HI) is commonly used to measure CPV-2-specific antibody levels in serum. However, the presence of nonspecific agglutinins in canine serum and artefactual precipitation of red blood cells (RBC) are both limitations of the assay. In this study, we compared the standard HI protocol with a refined HI protocol, in which canine serum was pre-incubated with porcine RBC for 12 h to remove nonspecific agglutinins and a lower concentration (0.1% vs. 0.8%) of porcine RBC suspensions was used to limit artefactual precipitation of RBC. A panel of canine sera, collected from 80 dogs of different ages and with different neutralising antibody titres, was analysed. Nonspecific agglutinins were identified in most (97%) serum samples from puppies4 months of age and in only 7% dogs 6 months old. Pre-treatment of serum samples was effective in removing nonspecific agglutinins from all samples and artefactual precipitation of RBCs was not noted when 0.1% RBC suspensions were used. Refinement of the HI protocol has increased the accuracy of interpretation and reduced the interference of nonspecific agglutinins, primarily seen in puppies. This reduces the likelihood of incorrect assessment of passive or active immunity in puppies when deciding whether to administer or defer vaccination, which could potentially leave them susceptible to CPV-2 infection.

Background Investigations of antimicrobial use in companion animals are limited. With the growing recognition of the need for improved antimicrobial stewardship, there is urgent need for more detailed understanding of the patterns of antimicrobial use in this sector. Objectives To investigate antimicrobial use for medical and surgical conditions in dogs and cats by Australian veterinarians. Methods A cross-sectional study was performed over 4 months in 2011. Respondents were asked about their choices of antimicrobials for empirical therapy of diseases in dogs and cats, duration of therapy, and selection based on culture and susceptibility testing, for common conditions framed as case scenarios: 11 medical, 2 surgical, and 8 dermatological. Results A total of 892 of the 1,029 members of the Australian veterinary profession that completed the survey satisfied the selection criteria. Empirical antimicrobial therapy was more common for acute conditions (76%) than chronic conditions (24%). Overall, the most common antimicrobial classes were potentiated aminopenicillins (36%), fluoroquinolones (15%), first- and second-generation cephalosporins (14%), and tetracyclines (11%). Third-generation cephalosporins were more frequently used in cats (16%) compared to dogs (2%). Agreement with Australasian Infectious Disease Advisory Panel (AIDAP) guidelines (generated subsequently) was variable ranging from 0 to 69% between conditions. Conclusions and Clinical Importance Choice of antimicrobials by Australian veterinary practitioners was generally appropriate, with relatively low use of drugs of high importance, except for the empirical use of fluoroquinolones in dogs, particularly for otitis externa and 3rd-generation cephalosporins in cats. Future surveys will determine whether introduction of the 2013 AIDAP therapeutic guidelines has influenced prescribing habits.

Canine disseminated fungal infection by Aspergillus species carries a guarded to grave prognosis as they often rapidly progress and are refractory to treatment with many euthanased soon after diagnosis. This case report describes a 2.5 year old female spayed German Shepherd Dog diagnosed with disseminated Aspergillus deflectus infection for which definitive treatment was declined by the owners. With only palliative management the dog survived three years and two months before succumbing to chronic kidney disease. Keywords: Aspergillus deflectus, Disseminated aspergillosis, Palliative care, Survival

In 2015, over 850,000 people died from chronic hepatitis and hepatocellular carcinoma (HCC) caused by hepatitis B virus (HBV). A novel hepatitis B-like virus has recently been identified in domestic cats. The pathogenic potential of domestic cat hepadnavirus (DCH), for which 6.5% to 10.8% of pet cats are viremic, is unknown. We evaluated stored formalin-fixed, paraffin-embedded biopsies of diseased and normal feline liver for the presence of DCH using PCR and in situ hybridization (ISH). DCH was detected in 43% (6/14) of chronic hepatitis cases and 28% (8/29) of HCCs, whereas cholangitis (n = 6), biliary carcinoma (n = 18) and normal liver (n = 15) all tested negative for DCH. Furthermore, in DCH-associated cases, the histologic features of inflammation and neoplasia, and the viral distribution on ISH were strikingly similar to those seen with HBV-associated disease. Several histological features common in human HBV-associated hepatitis, including piecemeal necrosis and apoptotic bodies, were identified in DCH-positive cases of chronic hepatitis. In two cases of HCC examined, the proliferation index in regions that were ISH-positive was higher than in ISH-negative regions. The intracellular distribution of virus in both hepatitis and HCC demonstrated that viral nucleic acid is present in both nuclear and cytoplasmic forms. Collectively, these findings demonstrate a compelling association between DCH and some cases of chronic hepatitis and hepatocellular carcinoma in the cat that mirrors features of HBV-associated hepatopathies. Future investigations of viral epidemiology and natural history are needed to establish the impact of DCH on feline health.

The past decade has seen an increase in aspergillosis in humans and animals due to Aspergillus viridinutans species complex members. Azole resistance is common to these infections, carrying a poor prognosis. cyp51A gene mutations are the main cause of acquired azole resistance in Aspergillus fumigatus. This study aimed to determine if the azole-resistant phenotype in A. viridinutans complex members is associated with cyp51A mutations or extrolite profiles., The past decade has seen an increase in aspergillosis in humans and animals due to Aspergillus viridinutans species complex members. Azole resistance is common to these infections, carrying a poor prognosis. cyp51A gene mutations are the main cause of acquired azole resistance in Aspergillus fumigatus. This study aimed to determine if the azole-resistant phenotype in A. viridinutans complex members is associated with cyp51A mutations or extrolite profiles. The cyp51A gene of clinical and environmental isolates was amplified using novel primers, antifungal susceptibility was tested using the Clinical and Laboratory Standards Institute methodology, and extrolite profiling was performed using agar plug extraction. Very high azole MICs were detected in 84% of the isolates (31/37). The MICs of the newer antifungals luliconazole and olorofim (F901318) were low for all isolates. cyp51A sequences revealed 113 nonsynonymous mutations compared to the sequence of wild-type A. fumigatus. M172A/V and D255G, previously associated with A. fumigatus azole resistance, were common among all isolates but were not correlated with azole MICs. Two environmental isolates with nonsusceptibility to itraconazole and high MICs of voriconazole and isavuconazole harbored G138C, previously associated with azole-resistant A. fumigatus. Some novel mutations were identified only among isolates with high azole MICs. However, cyp51A homology modeling did not cause a significant protein structure change for these mutations. There was no correlation between extrolite patterns and susceptibility. For A. viridinutans complex isolates, cyp51A mutations and the extrolites that they produced were not major causes of antifungal resistance. Luliconazole and olorofim show promise for treating azole-resistant infections caused by these cryptic species.

Hepadnaviruses infect several animal species. The prototype species, human hepatitis B virus (HBV), increases the risk of liver diseases and may cause cirrhosis and hepatocellular carcinoma. Recently a novel hepadnavirus, similar to HBV, has been identified through transcriptomics studies in a domestic cat with large cell lymphoma in Australia. Herewith, a collection of 390 feline serum samples was screened for hepadnavirus. Overall, the virus was identified in 10.8% of the sera with a significantly higher prevalence (17.8%) in the sera of animals with a clinical suspect of infectious disease. Upon genome sequencing, the virus was closely related (97.0% nt identity) to the prototype Australian feline virus Sydney 2016. The mean and median values of hepadnavirus in the feline sera were 1.3 × 106 and 2.1 × 104 genome copies per mL (range 3.3 × 100–2.5 × 107 genome copies per mL). For a subset of hepadnavirus-positive samples, information on the hemato-chemical parameters was available and in 10/20 animals a profile suggestive of liver damage was present. Also, in 7/10 animals with suspected hepatic disease, virus load was >104 genome copies per mL, i.e. above the threshold considered at risk of active hepatitis and liver damage for HBV.

Background Captivity presents extreme lifestyle changes relative to the wild, and evidence of microbiome dysbiosis in captive animals is growing. The gut microbiome plays a crucial role in host health. Whilst captive breeding and subsequent reintroduction to the wild is important for conservation, such efforts often have limited success. Post-release monitoring is essential for assessing translocation success, but changes to the microbiome of released individuals are poorly understood. The Tasmanian devil was previously shown to exhibit loss of microbiome diversity as a result of intense captive management. This current study examines changes in the devil gut microbiome in response to translocation and aims to determine if perturbations from captivity are permanent or reversible. Methods Using 16S rRNA amplicon sequencing, we conducted temporal monitoring of the gut microbiome of released devils during two translocation events, captive-to-wild and wild-to-wild. To investigate whether the microbiome of the released devils changed following translocation, we characterized their microbiome at multiple time points during the translocation process over the course of 6–12 months and compared them to the microbiome of wild incumbent devils (resident wild-born devils at the respective release sites). Results We showed that the pre-release microbiome was significantly different to the microbiome of wild incumbent animals, but that the microbiomes of animals post-release (as early as 3 to 4 weeks post-release) were similar to wild incumbents. The gut microbiome of released animals showed significant compositional shifts toward the wild incumbent microbiome of both translocation events. Conclusion Our results suggest that the devil gut microbiome is dynamic and that loss of microbiome diversity in captivity can be restored following release to the wild. We recommend the broader application of microbiome monitoring in wildlife translocation programs to assess the impacts of translocation on animal microbiomes.

Case summary Two 13-year-old domestic shorthair cats were diagnosed with unilateral right adrenocortical carcinomas (ACCs) and primary hyperaldosteronism (PHA). Both had polyuria, polydipsia and weight loss, and developed severe anaemia from an episode of acute adrenal haemorrhage. In one case, this occurred during hospitalisation and treatment of severe muscle weakness with cervical ventroflexion, while the other cat had acute collapse at home. A diagnosis of PHA was confirmed in both cases based on measurement of plasma aldosterone and renin activity. In one case, basal progesterone was also measured and was elevated. On ultrasonography and CT in one case, haemorrhage into the right retroperitoneal space was identified. Unilateral adrenalectomy was performed in both cases and there was no evidence of venous tumoral invasion in either. On histopathology of the excised adrenal glands both were ACCs with tumour necrosis, and one had extensive intratumoral haemorrhage. Both cats were diagnosed with International Renal Interest Society stage 2 or 3 chronic kidney disease postoperatively; one survived for 18 months and the other was well 8 months postoperatively. Relevance and novel information Acute adrenal haemorrhage secondary to adrenal neoplasia has been reported in only one other cat, in which tumour type and function were not specified. Acute adrenal haemorrhage can occur as a consequence of tumour necrosis and rupture and can cause severe hypovolaemia and anaemia in cats with primary hyperaldosteronism.

Case summary A 12-year-old male neutered Tonkinese cat was presented for acute ataxia, weakness, altered mentation and generalised tremors. The cat had been administered oral spinosad (140 mg; 33.5 mg/kg) 48 h prior to the onset of clinical signs, and an oral anthelmintic containing milbemycin oxime (16 mg; 3.8 mg/kg) and praziquantel (40 mg; 9.6 mg/kg) 12 h before the onset of clinical signs. On physical examination, dull-to-obtunded mentation, tetraparesis, ataxia and mild tremors of facial, limb and trunk muscles were noted. Serum biochemical changes and urinalysis were consistent with haemoconcentration. The results of a complete blood count, urine culture and serology for feline leukaemia virus, feline immunodeficiency virus and cryptococcal antigen were negative. The patient was monitored in hospital and all clinical signs resolved within 24 h. Relevance and novel information The neurological signs in this case were consistent with macrocyclic lactone neurotoxicity, which is suspected to have occurred from an adverse drug interaction between spinosad and milbemycin oxime. This report serves to highlight the potential for this adverse drug interaction between these commonly used prophylactic drugs.

The domestic cat is natural host to both feline immunodeficiency virus and Felis catus gammaherpesvirus 1 (FcaGHV1). Comparative data suggest that these agents might act as synergistic copathogens in feline AIDS-related lymphoma. To identify leucocyte subsets harbouring gammaherpesvirus DNA, whole blood from 5 healthy, FcaGHV1-infected cats was labelled with monoclonal antibodies to feline CD21, CD4, CD8 and CD14 for 4-way fluorescence-activated cell sorting. FcaGHV1gB qPCR was performed on DNA extracted from purified fractions and whole blood longitudinally. FcaGHV1 DNA was detected in CD21+, CD4+, CD8+, but not CD14+ cells. Variation in whole blood load, up to 19,788 copies/10(6)cells, was detected in individual cats over time. FcaGHV1 DNA was undetectable in one cat on one occasion highlighting that qPCR of whole blood from a single time point will not detect all cases of FcaGHV1 infection. Further investigation of the role of FcaGHV1 in feline lymphoid malignancies is warranted.

Whether Toxoplasma gondii genotype is associated with disease severity in naturally occurring toxoplasmosis in domestic cats is unknown. The aim of this study was to compare genotypes of T. gondii in latently infected cats with those in cats with clinical toxoplasmosis. Results of a PCR targeting the B1 gene to detect T. gondii DNA were positive in tissue samples from 11 of 17 (65%) seropositive cats tested including four with clinical toxoplasmosis and seven with latent infections, as determined by serology, histologic findings and immunohistochemistry. Three of the four cats with clinical toxoplasmosis were immunosuppressed. Complete genotyping was performed in seven cats using PCR-RFLP at 12 loci (SAG1, 5'SAG2 and 3'SAG2, altSAG2, SAG3, BTUB, GRA6, c22-8, c29-2, L358, PK1 and Apico) and direct sequencing of the multi-copy B1 gene. Partial genotyping using six loci was performed in one cat with latent infection. T. gondii type II (ToxoDB genotype #3) was determined in four cats with clinical toxoplasmosis and three cats with latent toxoplasmosis Novel T. gondii B1 gene polymorphisms were detected in two strains (at nucleotide posititions 233, 366 and 595) and a B1 gene polymorphism unique to Australia was identified in another (guanine/adenine at nucleotide position 378). One cat was co-infected with two or more type-II like strains at 3'SAG2. The results of this study suggest that the infecting T. gondii genotype, based on these 12 loci, is not a determinant of clinical disease in cats naturally infected with T. gondii and type II strains are prevalent in Australia.

Background Serological tests for diagnosis of aspergillosis in immunocompetent humans and animals are based on Aspergillus-specific IgG (As-IgG). In humans with chronic pulmonary aspergillosis, As-IgA may be detectable even if IgG titers are negative. Cats with upper respiratory tract aspergillosis (URTA) have detectable As-IgG, but their ability to mount an IgA response and its diagnostic utility are unknown. Objectives To determine whether serum As-IgA can be detected in cats with URTA and evaluate its diagnostic utility alone or combined with As-IgG. Animals Twenty-three cats with URTA (Group 1), 32 cats with other respiratory diseases (Group 2), and 84 nonrespiratory controls (Group 3). Methods Serum As-IgA and As-IgG was measured by indirect ELISA. Optimal cutoff values were determined by receiver-operating curve analysis. Sensitivity (Se) and specificity (Sp) for URTA diagnosis were determined. Results Serum IgA was detected in 91.3% of Group 1 cats. The Se of IgA detection was 78.3% and Sp was 96.9% for Group 2, 85.7% for Group 3 and 88.8% for Group 2 and 3 combined. Assay Se for IgG was 100% and Sp was 92.2%. Using combined IgA and IgG results at cutoffs optimized for Sp for IgA and Se for IgG and combined controls (Groups 2 and 3), Se for diagnosis was 100% and Sp was 91.4%. Conclusion and Clinical Importance Most cats with URTA have serum As-IgA antibodies that can be detected by ELISA. Paired measurement of serum As-IgA and IgG shows no benefit for diagnosis of feline URTA over IgG alone.

Leucocyte populations in the sinonasal mucosa of cats with and without upper respiratory tract aspergillosis were compared using immunohistochemistry and computer-aided morphometry. Inflammation was identified in the nasal mucosa of all affected cats, comprising predominantly of lymphoplasmacytic infiltration of the lamina propria associated with epithelial proliferation and degeneration. There was intense and diffuse expression of class II antigens of the major histocompatibility complex, associated with sites of hyphal invasion with hyperplasia and ulceration of the epithelium adjacent to fungal elements. Significantly more CD79b(+) cells, total lymphocytes, immunoglobulin (Ig)-expressing cells and MAC387(+) cells infiltrated the epithelium and more IgG(+) cells and total Ig-expressing cells infiltrated the lamina propria in affected cats compared with controls. Importantly, the inflammatory profile in affected cats was not consistent with the T helper (Th)1 and Th17 cell-mediated response that confers protective acquired immunity against invasive aspergillosis in dogs and people and in murine models of the infection. This finding may help to explain the development of invasive aspergillosis in systemically immunocompetent cats.

Objective To determine whether the overall hemostasis potential (OHP) and calibrated automated thrombogram (CAT) were significantly different between dogs with thrombosis and normal dogs. Animals Ten dogs with clinical evidence of thromboembolic disease had both OHP and CAT performed. Forty healthy control dogs had OHP performed, and 23 of these also had CAT performed. Measurements and Main Results Dogs with thrombosis had significantly higher OHP (P = 0.003), overall coagulation potential (P = 0.0001), and maximum optical density (Max OD, P < 0.0001) than normal dogs, and a significantly longer delay in the start of clot formation (P = 0.01). Max OD was higher than established reference intervals in 80% of the dogs with thrombosis. Using the CAT assay, dogs with thrombosis had a significantly longer lag time than normal dogs (P < 0.001). Plasma fibrinogen concentration correlated positively with overall coagulation potential, OHP, Max OD, and the slope of the OHP curve (P < 0.05), and was increased in 90% of dogs with thrombosis. Conclusions The OHP assay findings were significantly different between normal dogs and those with thrombosis. CAT did not detect any significant differences between these populations of dogs, other than the lag time of the assay.

Canine parvovirus (CPV) is an important cause of disease in domestic dogs. Sporadic cases and outbreaks occur across Australia and worldwide and are associated with high morbidity and mortality. Whether transmission of CPV occurs between owned dogs and populations of wild dogs, including Canis familiaris, Canis lupus dingo and hybrids, is not known. To investigate the role of wild dogs in CPV epidemiology in Australia, PCR was used to detect CPV DNA in tissue from wild dogs culled in the peri-urban regions of two Australian states, between August 2012 and May 2015. CPV DNA was detected in 4.7% (8/170). There was a strong geospatial association between wild-dog CPV infections and domestic-dog CPV cases reported to a national disease surveillance system between 2009 and 2015. Postcodes in which wild dogs tested positive for CPV were 8.63 times more likely to also have domestic-dog cases reported than postcodes in which wild dogs tested negative (p = 0.0332). Phylogenetic analysis of CPV VP2 sequences from wild dogs showed they were all CPV-2a variants characterized by a novel amino acid mutation (21-Ala) recently identified in CPV isolates from owned dogs in Australia with parvoviral enteritis. Wild-dog CPV VP2 sequences were compared to those from owned domestic dogs in Australia. For one domestic-dog case located approximately 10 km from a wild-dog capture location, and reported 3.5 years after the nearest wild dog was sampled, the virus was demonstrated to have a closely related common ancestor. This study provides phylogenetic and geospatial evidence of CPV transmission between wild and domestic dogs in Australia.