Ventral dermatitis in rowi (Apteryx rowi) caused by cutaneous capillariasis.

In 2013 there was an outbreak of crusting ventral dermatitis among a group of juvenile rowi (Apteryx rowi), a species of the endangered New Zealand kiwi, that were being raised on an off-shore island sanctuary. Biopsies taken at the time found nematodes migrating within the epidermis of affected skin but the specific identity and origin of the organisms was not established, and sporadic cases of similar skin disease continue to occur on the island. On examination of additional sections from the original skin biopsies, adult nematodes and eggs were identified, the histomorphology of which was consistent with Capillaria sensu lato. PCR was performed on DNA extracted from archived formalin-fixed, paraffin-embedded tissue blocks of skin from eight affected rowi, using primers targeting the 18S region of nuclear ribosomal DNA and the COI gene of mitochondrial DNA of capillarid nematodes. The 18S sequences from all rowi samples were identical and matched sequences from members of the genus Eucoleus. In contrast, two distinct capillarid COI sequences were obtained, in one case both from the same rowi skin biopsy. While there were no close matches, both COI sequences also aligned nearest to sequences identified as Eucoleus spp. It is considered unlikely that two different nematode species are involved in the rowi skin lesions and the possible amplification of a COI pseudogene or "numt" is discussed. A species-level identification of the capillarid nematodes causing skin disease in rowi was not obtained, however based on histological evaluation the infections include reproductively-active adult nematodes. This finding indicates the possibility of perpetuation of the skin disease in the absence of the original source, as well as raising potential for the transfer of infection from the island when the juvenile rowi are translocated to their new habitats.

Nematode larva migrans caused by Toxocara cati in the North Island brown kiwi (Apteryx mantelli).

Sporadic cases of visceral and neural nematode larva migrans have been diagnosed at necropsy in the endangered New Zealand kiwi (Apteryx spp.), but the causative organisms have not yet been definitively identified. From an initial group of five affected kiwi, PCR was performed on DNA extracted from archival formalin-fixed paraffin-embedded tissue sections in which larval nematodes had been histologically identified. Sequencing of positive results from four out of the five kiwi aligned with sequences from Toxocara cati, a nematode parasite whose definitive host is the domestic cat. PCR was then performed on a second group of 12 kiwi that had histologic inflammatory lesions consistent with larva migrans, but variable larval presence. Repeatable positive PCR results were only achieved in one tissue, in which larval organisms were histologically confirmed. This study supports the use of PCR as an alternative or adjunct to the morphological identification of nematode larvae in formalin-fixed histopathological samples, as well as showing that in investigation of larva migrans, PCR has greatest chance of success from sections where nematode larvae are evident histologically. The identification of Toxocara cati from lesions of larva migrans in kiwi reflects an indirect, parasite-mediated effect of an invasive mammalian species on a native species.

Toxocara canis Larval Migration Causing Verminous Pneumonia in Fading Puppies From 2 Scottish Terrier Litters.

Migration of vertically transmitted Toxocara canis larvae through the liver and lungs is poorly documented as a cause of periparturient mortality in puppies. This case series describes 4 cases of fading puppies in 2 litters from 2 different bitches owned by the same breeder. Of the 4 cases, 4 had verminous pneumonia, 2 had fibrinoid necrosis of pulmonary arterioles, 4 had hepatic necrosis and inflammation, 2 had hepatic thrombophlebitis, and 1 had tracheal occlusion. These lesions were associated with migrating nematode larvae morphologically consistent with T. canis. The identity of the larvae was confirmed by sequencing of a portion of the ITS-2 region of nuclear ribosomal DNA. The tissues involved are consistent with the known migration pathways of this parasite. The dam of the first litter was negative for Toxocara spp. and other intestinal parasites by fecal floatation. This report highlights the need to consider T. canis migration in the differential diagnosis of fading puppies.

Serum Fructosamine Concentration in Uncontrolled Hyperthyroid Diabetic Cats Is within the Population Reference Interval.

Diabetes mellitus is a common endocrinopathy of cats that is characterized by persistent fasting hyperglycemia. However, stress induces substantial hyperglycemia in cats that poses a challenge to the veterinarian who may wrongly interpret the high serum concentration of blood glucose as evidence of diabetes mellitus. Fructosamine is a glycated serum protein that serves as an index of glycemic control in cats and is useful because it is not affected by stress hyperglycemia. However, factors such as body weight, hypoproteinemia, and increased serum thyroid hormone concentration can alter fructosamine concentration. The goal of this retrospective study was to compare the fructosamine concentrations in diabetic and nondiabetic cats with and without uncontrolled hyperthyroidism. A secondary goal was to determine the effect of sex, age, different populations of cats, and diabetes on the variability of fructosamine. We found that the mean (±SE) serum fructosamine of hyperthyroid diabetic cats (332 ± 24 µmol/L, 95% CI 291-379 µmol/L) was within the population-based reference interval (200-360 µmol/L) and significantly lower in comparison to euthyroid diabetic cats (527 ± 10 µmol/L, 95% CI 515-553 µmol/L). Additionally, in this study, diabetes accounted only for approximately 50% of the variance in serum fructosamine, while age, sex, and population made a minor contribution to this variance. In conclusion, finding serum fructosamine that is within the population-based reference interval in an uncontrolled diabetic cat should alert the veterinarian to the possibility of concurrent hyperthyroidism. Additionally, the veterinary clinician should consider that serum fructosamine might be substantially affected by factors other than diabetes.

Detection of DNA sequences from a novel papillomavirus in a feline basal cell carcinoma.

BACKGROUND: Basal cell carcinomas (BCCs) are uncommon feline skin neoplasms of uncertain cause. CASE: A 14-year-old Abyssinian cat developed a soft dermal nodule on the dorsal thorax. This mass grew slowly over a six month period before being surgically excised. METHODS AND RESULTS: Histology revealed a BCC. Additionally, changes suggestive of an early Bowenoid in situ carcinoma (BISC) were present in the overlying epidermis. Both the BCC and the BISC contained papillomavirus-induced cell changes and prominent basophilic intracytoplasmic bodies. PCR using consensus primers and primers specific for Felis catus papillomavirus types 2 and 3 (FcaPV-2 and -3) was used to amplify papillomaviral DNA. The same papillomaviral DNA sequence was present in the BCC and the BISC. This sequence was most similar to FcaPV-3, but with just 70.5% similarity, was from a novel papillomavirus type. No recurrence or further masses developed. CONCLUSIONS: This case is unusual due to the presence of a large dermal BCC associated with minimal BISC changes in the overlying epidermis. Additionally, papillomavirus-induced cell changes have not been described previously in a BCC. Furthermore, both the BCC and the BISC contained sequences from a novel papillomavirus type. These observations suggest that the development of some BCCs could be influenced by papillomavirus infection. The novel papillomavirus type detected is the third papillomavirus type to be associated with skin cancer in cats.

Clinical, histological and prognostic features of a novel nail-bed lesion of cats: 41 cases.

Objectives There is a distinct subset of lesions arising on the digits of cats, located at or close to the nail-bed epithelium, which are typically composed of proliferative fibroblast-like cells, multinucleate giant cells and areas of osseous metaplasia, but currently there is no published literature detailing the clinical or histological features of these lesions. Methods This study identified 41 such cases from two large commercial diagnostic laboratories and assessed various histological and clinical features; 22 cases had additional follow-up data available. Results All masses in this study were exophytic, variably inflamed, contained large numbers of spindle cells and had areas of capillary formation. The majority also had areas of ulceration, multinucleate giant cells and osseous metaplasia. The mitotic count was variable, but mitoses were confined to the fibroblast-like cells. Male cats appeared predisposed and the second digit was the most commonly affected. Conclusions and relevance These distinctive lesions arising on the digits of cats had potential for local recurrence but metastasis was not reported. Based on these clinical and histological features, the masses in this study appear most similar to giant cell reparative granulomas, and trauma, injury to the nail or nail-bed and nail-bed infections may potentially contribute to their development.

Bowenoid in situ carcinomas in two Devon Rex cats: evidence of unusually aggressive neoplasm behaviour in this breed and detection of papillomaviral gene expression in primary and metastatic lesions.

BACKGROUND: Bowenoid in situ carcinomas (BISCs) are rare feline tumours that are thought to be caused by papillomavirus infection. Although they usually develop in old cats and are slowly progressive, multiple aggressive BISCs have been reported previously in a comparatively young Devon Rex cat. ANIMALS: A 5-year-old (Case 1) and an 8-year-old (Case 2) Devon Rex cat developed numerous BISCs. Rapid progression resulted in euthanasia of both cats after 8 months. A postmortem examination was possible only for Case 2 and revealed pulmonary metastases. METHODS AND RESULTS: Consensus PCR amplified only Felis catus papillomavirus type 2 (FcaPV-2) DNA from lesions from both cats. High FcaPV-2 copy number and FcaPV-2 E6/E7 gene expression were detected in a BISC from Case 1. High FcaPV-2 copy number and FcaPV-2 gene expression were detected in a BISC, a cutaneous squamous cell carcinoma (SCC) and the pulmonary metastases from Case 2, but not in two other cutaneous SCCs. CONCLUSIONS: The results provide additional evidence that BISCs develop at a younger age in Devon Rex cats and that BISCs in Devon Rex cats have a more aggressive behaviour than BISCs in other cat breeds. These unusual features should be considered when evaluating and treating skin disease in Devon Rex cats. The detection of FcaPV-2 gene expression in the lung neoplasms suggests a potential role of FcaPV-2 in the development of metastatic disease. However, the absence of FcaPV-2 gene expression in two cutaneous SCCs suggests that other factors could have also promoted cancer development.

Molecular and immunohistochemical studies do not support a role for papillomaviruses in canine oral squamous cell carcinoma development.

Oral squamous cell carcinomas (OSCCs) are common neoplasms of dogs and are of unknown cause. Whereas papillomaviruses (PVs) are an established cause of human OSCCs, few studies have investigated canine OSCCs for a PV aetiology. In humans, a PV aetiology can be determined by detecting PV DNA and PV-induced increased p16(CDKN2A) protein (p16) within the OSCC. In this study, PCR, using four different primer sets and p16 immunohistochemistry, was used to evaluate 28 canine OSCCs for a possible PV aetiology. None of the primers amplified PV DNA from any of the OSCCs although four neoplasms contained intense p16 immunostaining. Intense p16 immunostaining would indicate a PV aetiology in a human OSCC but the absence of PV DNA suggests that the increase in p16 was not due to PV infection. Overall the results indicated that PVs are not a significant cause of canine OSCCs.

Felis catus papillomavirus types 1 and 4 are rarely present in neoplastic and inflammatory oral lesions of cats.

Oral squamous cell carcinomas (OSCCs) are common feline cancers. Why OSCCs are so common in cats is unknown; however, 25% of human OSCCs are caused by papillomaviruses (PVs). Two feline oral PVs (FcaPV-1 and 4) are recognized. As PVs are highly host and location specific, if PVs do cause feline OSCCs, FcaPV-1 and 4 are the most likely etiological agents. PCR primers specific for FcaPV-1 amplified DNA from 1 of 36 feline OSCCs and 1 of 16 inflammatory oral lesions. No DNA was amplified by primers specific for FcaPV-4. PV DNA was not amplified from any additional sample using consensus primers. No PV cytopathology was visible in the OSCC that contained FcaPV-1 DNA, but viral cytopathology was present in a focus of epithelial hyperplasia in the non-neoplastic sample. This study does not support a PV etiology of feline OSCCs, but shows that FcaPV-1 can asymptomatically infect the mouth of cats.

Infrequent detection of papillomaviral DNA within canine cutaneous squamous cell carcinomas, haemangiosarcomas and healthy skin on the ventrum of dogs.

BACKGROUND: Canine squamous cell carcinomas (SCCs) most frequently develop on the ventral abdomen and are thought to be caused by ultraviolet (UV) light. Papillomaviruses (PVs) have been associated with cutaneous SCCs in multiple species, including dogs. HYPOTHESIS: That PVs act as cofactors in canine UV-induced SCCs. ANIMALS: The study was performed on skin from the ventrum of 60 dogs. These samples included 20 SCCs, 20 haemangiosarcomas and 20 samples of clinically normal skin. Two canine viral plaques were included as positive controls for PV. METHODS: PCR was used to amplify PV DNA from all samples. Primers used included two sets of consensus primers and two sets of primers that were designed specifically to amplify PV DNA sequences detected in the viral plaques. RESULTS: The MY09/11 consensus primers amplified PV DNA from both viral plaques. One plaque contained a DNA sequence (CfPV-JM) that had been previously reported from a dog with multiple cutaneous SCCs. The other plaque contained a previously unreported PV DNA sequence. No PV DNA was amplified by either consensus primer from any of the ventrum skin samples. Primers designed specifically to amplify the CfPV-JM sequence amplified DNA from one SCC, but no other sample. No PV DNA was amplified using the other specific PCR primer set. CONCLUSIONS AND CLINICAL IMPORTANCE: These results do not support a significant role for PVs in SCC development from the ventrum of dogs. However, they contribute another PV sequence to the list of PVs that have been associated with viral plaque development in dogs.

Development of an injection site sarcoma shortly after meloxicam injection in an unvaccinated cat.

A single dose of a rapidly-absorbed non-steroidal anti-inflammatory drug (NSAID) was injected into the subcutaneous tissue of the interscapular region of a 12.5-year-old cat. A mild swelling was noticed at the injection site 6 weeks later. This progressed into a 5 cm diameter mass which was removed 6 months after the injection had been given. An injection site sarcoma (ISS) was diagnosed histologically. As the cat had not been vaccinated for at least 12 years, the previous NSAID injection was considered to be a possible cause of the ISS. Inflammation is thought to be important in the development of ISS. If injection of a rapidly-absorbed NSAID can stimulate sufficient inflammation to promote the development of an ISS, other non-vaccine injections may also have the potential to influence ISS development. This suggests that injection of both vaccines and non-vaccine medications should be minimised to reduce the risk of ISS development.

Papillomaviral DNA and increased p16CDKN2A protein are frequently present within feline cutaneous squamous cell carcinomas in ultraviolet-protected skin.

Squamous cell carcinomas (SCCs) are common feline skin tumours. While exposure to ultraviolet (UV) light causes some SCCs, a subset develop in UV-protected skin. In cats, papillomaviruses (PVs) cause viral plaques and Bowenoid in situ carcinomas (BISCs). As both may progress to SCC, it was hypothesized that SCCs in UV-protected skin may represent neoplastic transformation of a PV-induced lesion. To investigate this hypothesis, PCR was used to amplify PV DNA from 25 UV-protected and 45 UV-exposed SCCs. Oncogenic human PVs cause neoplasia by mechanisms that also increase p16(CDKN2A) protein (p16). As increased p16 is present in feline viral plaques and BISCs, immunohistochemistry was used to detect p16 within the SCCs. Papillomaviral DNA was amplified from 76% of UV-protected SCCs, but only 42% of UV-exposed SCCs. Increased p16 was present in 84% of UV-protected SCCs, but only 40% of UV-exposed SCCs. The more frequent detection of PV DNA and increased p16 within UV-protected SCCs supports the hypothesis that some develop from a PV-induced plaque or BISC. Felis domesticus PV-2 is thought to cause viral plaques and BISCs. This PV was detected most frequently within the UV-protected SCCs, supporting development from a PV-induced lesion. Increased p16 and PV DNA were less frequent within UV-exposed SCCs, presumably because these developed from actinic keratosis rather than a PV-induced lesion. The results support the hypothesis that some feline cutaneous SCCs are caused by PV infection and suggest that PVs may cause neoplasia by mechanisms that also increase p16.

Evaluation of feline oral squamous cell carcinomas for p16CDKN2A protein immunoreactivity and the presence of papillomaviral DNA.

Oral squamous cell carcinomas (OSCCs) develop commonly in cats. While the cause of the feline neoplasms is unknown, a quarter of human OSCCs are caused by papillomavirus (PV) infection. As PV DNA has been previously detected in a feline OSCC, it was hypothesised that PV infection could be a significant cause of feline OSCCs. Human OSCCs that are caused by PVs contain increased p16(CDKN2A) protein (p16), which can be detected using immunohistochemistry. In cats, increased p16 immunoreactivity has been reported within PV-associated skin lesions. This study evaluated p16 immunoreactivity within 30 feline OSCCs. Additionally, PCR was used to amplify PV DNA from the OSCCs. Increased p16 immunoreactivity was present within 2 OSCCs. However, as PV DNA was not amplified from any OSCC in this study, it cannot be confirmed that the increased p16 was caused by PV infection. Therefore, these results do not support the hypothesis that PVs are a significant cause of OSCCs in cats. Loss of p16 expression is considered an important process in the development of human non-PV-induced OSCCs. In contrast, loss of p16 immunoreactivity was only present in 2 feline OSCCs. This suggests that human and feline OSCCs develop due to different molecular mechanisms.

Amplification of papillomaviral DNA sequences from a high proportion of feline cutaneous in situ and invasive squamous cell carcinomas using a nested polymerase chain reaction.

Squamous cell carcinomas (SCCs) are common skin tumours of cats. Previous studies have suggested that papillomaviral (PV) DNA is detectible within some feline SCCs. A PV DNA sequence has been previously amplified from five feline bowenoid in situ carcinomas (BISCs). Primers specific for this sequence were used in a nested polymerase chain reaction to compare PV detection rates in SCCs to rates within non-SCC skin lesions. Papillomaviral DNA was amplified from 20 of 20 BISC, 17 of 20 invasive SCC and 3 of 17 non-SCC controls. The rate of PV amplification from feline cutaneous SCCs was significantly higher than from non-SCC lesions. These results confirm that feline cutaneous SCCs are associated with PV infection. In humans, there is evidence that PVs promote SCC development within sun-exposed skin. The demonstrated association between PVs and feline cutaneous SCCs suggests, but does not prove, that PVs may also promote feline SCC development. If PVs are oncogenic in cats, prevention of PV infection may reduce feline cutaneous SCC development. To the authors' knowledge, this is the first time that PV DNA has been amplified from a non-SCC sample of feline skin.

Renal cystadenoma in a domestic shorthair.

An 11-year-old domestic shorthair was examined after an enlarged left kidney was palpated by the referring veterinarian. No abnormalities were noted on complete blood count, serum biochemical profile and total thyroxine concentration, and the urine specific gravity was 1.039. An abdominal ultrasound identified the presence of a large cystic structure on the caudal pole of the left kidney. No abnormalities of the right kidney were seen. A left ureteronephrectomy was performed, and the cat recovered uneventfully from the procedure and was discharged from the hospital 5 days after surgery. The cat remains clinically normal 16 months postoperatively. Histopathology of the removed kidney demonstrated the presence of a renal cystadenoma. This report describes the successful surgical treatment of a renal cystadenoma. Renal cystadenoma should be considered as a differential diagnosis when renomegaly is noted. To the author's knowledge, a renal cystadenoma has not been previously reported in a cat.

Detection of papillomaviral sequences in feline Bowenoid in situ carcinoma using consensus primers.

Feline Bowenoid in situ carcinoma (BISC) is a rare disease that presents as multiple discrete plaques of epidermal hyperplasia and dysplasia. Two studies using immunohistochemistry revealed papillomaviral antigens in 11% and 47% of BISCs. Additionally, a recent study detected papillomaviral DNA in 24% of BISC lesions. To further investigate the association between papillomaviruses and BISC, polymerase chain reaction using consensus primers was used to detect papillomaviral DNA in 18 formalin-fixed samples of BISC. Papillomaviral DNA was amplified from 11 of the samples but from none of the controls. Six amplicons were sequenced; one was homologous with a papillomavirus from a human patient with multiple cutaneous squamous cell carcinomas and the other five showed weak homology to human papillomavirus type 17. These five sequences were > 96% homologous over a 235 bp sequence, indicating the presence in all five BISCs of one papillomavirus type distinct from any previously sequenced and more closely related to human than animal papillomaviruses. The results confirm an association between BISC and papillomaviruses, and as all six papillomavirus sequences identified are closely related to human papillomaviruses, it is possible that the virus is transmitted from humans to cats or vice versa.

Multiple myeloma in 16 cats: a retrospective study.

BACKGROUND: There is limited published information regarding feline multiple myeloma. Diagnostic criteria are derived from canine studies and to our knowledge, have not been critically reviewed for cats. OBJECTIVE: To evaluate the clinical and laboratory findings in cats with multiple myeloma and appraise diagnostic criteria. METHODS: Retrospective evaluation of medical records was performed. Inclusion required an antemortem diagnosis of multiple myeloma using 2 of 4 criteria: 1) >or=20% plasma cells in the bone marrow, or >or=10% if atypical plasma cells; 2) paraproteinemia; 3) radiographically-evident osteolysis; 4) light chain proteinuria. Alternatively, a postmortem diagnosis was based on the findings of multiple plasma cell neoplasms, with marrow involvement. RESULTS: Sixteen cats were diagnosed with multiple myeloma between 1996 and 2004, with a median age of 14.0 years; 9 of 16 (56%) were castrated males, and 7 of 16 (44%) were spayed females. Laboratory abnormalities included hyperglobulinemia (14/16, 87.5%), with 11/14 (78.5%) monoclonal and 3/14 (21.4%) biclonal gammopathies; hypoalbuminemia (4/16, 25%); light chain proteinuria, (4/9, 44.4%); hypocholesterolemia (11/16, 68.7%); hypercalcemia, (3/15, 20%); nonregenerative anemia, (11/16, 68.7%); regenerative anemia, (1/16, 6.2%); neutropenia (5/15, 33.3%); thrombocytopenia (8/16, 50%); and marrow plasmacytosis (14/15, 93.3%). Plasma cells were markedly immature, atypical, or both in 10 of 12 (83.3%) cats. Focal or multifocal osteolysis was noted in 6 of 12 (50%) cats for which radiographs were available for review; generalized osteopenia was found in 1 (8.3%) cat. Noncutaneous, extramedullary tumors were found in all cats assessed, 7/7 (100%), including spleen (6), liver (3), and lymph nodes (4). The disease in 1 of 2 cats with cutaneous tumors progressed to plasmacytic leukemia. CONCLUSIONS: Common findings in feline multiple myeloma include atypical plasma cell morphology, hypocholesterolemia, anemia, bone lesions, and multi-organ involvement. Based on the results of this study, we advocate modifying diagnostic criteria in cats to include consideration of plasma cell morphology and visceral organ infiltration.