Intracoelomic Teratoma in an Eclectus Parrot (Eclectus roratus).

A 26-year-old, male eclectus parrot (Eclectus roratus) was presented to its primary care veterinarian for a 10-day history of increased respiratory effort, lethargy, and a single episode of regurgitation. Hepatomegaly, proventricular enlargement, cranial displacement of the ventriculus, and coelomic effusion were suspected based on a 1-view radiographic image, and the patient was referred for further evaluation. On presentation to the referral veterinary hospital, a distended coelom and dyspnea with abnormal respiratory sounds were abnormalities noted upon physical examination of the patient. The bird was hospitalized for supportive care, and diagnostic tests were performed. Initial radiographic images at the referral hospital revealed a large intracoelomic mass. A computed tomographic scan was performed; however, the origin of the mass could not be determined. A fine-needle aspirate and cytologic evaluation of the intracoelomic mass revealed a neoplastic process but no specific tissue type. Two days after presentation to the referral hospital, an exploratory coeliotomy to surgically resect the mass was attempted. The mass occupied most of the coelomic cavity, with multiple adhesions to internal organs. The mass was successfully resected; however, the patient destabilized and died despite resuscitation efforts. Histopathologic examination of submitted tissue from the mass with immunohistochemistry revealed mixed populations of neoplastic cells differentiated from 3 primordial germinal layers, confirming the diagnosis of teratoma. Teratomas appear to be a rare tumor in avian species but should be included in a list of differential disease diagnoses for abnormal tissue masses of unknown origin. Only 2 cases of teratomas have, to our knowledge, been reported in psittacine species.

Myocardial transcription of inflammatory and remodeling markers in cats with hypertrophic cardiomyopathy and systemic diseases associated with an inflammatory phenotype.

Feline hypertrophic cardiomyopathy (HCM) is characterized by macrophage-driven myocardial remodeling processes in a pro-inflammatory environment. To further investigate the mechanisms behind these processes, the myocardial transcription of cytokines and remodeling enzymes was comparatively assessed in cats with HCM and cats without cardiac diseases. Sixty-seven cats were included, 17 cats with HCM (including 5 with atrial thrombus; AT), and 50 cats without cardiac diseases. The latter comprised 10 control cats (no cardiac or relevant systemic disease), 34 cats with diseases suspected to be associated with a systemic inflammatory state of which 18 suffered from feline infectious peritonitis (FIP), and 6 cats with multicentric lymphoma. Samples from atria, ventricular free walls and interventricular septum were examined using quantitative reverse transcriptase PCR. The overall highest myocardial marker transcriptions were observed in cats with multicentric lymphoma, FIP and HCM, followed by diseases likely associated with a systemic inflammatory state, and control cats. Inflammatory marker transcription predominated in the myocardium of cats with systemic inflammatory diseases, whereas in HCM the transcription of remodeling enzymes prevailed. Sex significantly influenced the myocardial transcription of several remodeling enzymes. These results suggest a versatile myocardial response depending on the disease and illustrates the relevance of sex for the cardiac response to cardiac and systemic disease in cats. A systemic inflammatory state appears to elicit an inflammatory phenotype in the myocardium, whereas in HCM, the myocardium mediates its own remodeling. In HCM, the identified markers might be involved in the ongoing remodeling processes causing structural and functional changes.

Presumptive malignant transformation of chronic polypoid cystitis into an apical transitional cell carcinoma without BRAF mutation in a young female dog.

A 3-year-old spayed female English Springer Spaniel was presented twice 4 months apart for investigation of hematuria and pollakiuria without urinary tract infection. Both ultrasound examinations identified a stable craniodorsal bladder wall thickening. The first cystoscopic biopsy samples indicated lymphoplasmacytic cystitis and the second polypoid cystitis. The dog was represented 8 months later for recurrent clinical signs despite medical management. Although the ultrasound examination showed stable disease, repeat cystoscopic biopsy identified transitional cell carcinoma (TCC), confirmed on tissue removed by partial cystectomy. No BRAF mutation was ever detected in urine or tissue samples. To our knowledge, this case represents the first report of presumptive malignant transformation of polypoid cystitis into an apical TCC in a dog. Dogs with polypoid cystitis should be followed closely and surgical management considered if rapid resolution is not achieved with medical management.

Aberrant Mesenteric Migration of Spirocerca lupi Larvae Causing Necrotizing Eosinophilic Arteritis, Thrombosis, and Intestinal Infarction in Dogs.

This report presents a novel canine condition in 32 dogs in which aberrant migration of Spirocerca lupi larvae through mesenteric arteries, instead of gastric arteries, led to small or large intestinal infarction. This form of spirocercosis was first recognized in Israel in 2013 and is currently ongoing. Typical clinical signs were anorexia and weakness of 3 to 4 days and, less frequently, vomiting and diarrhea, followed by collapse, bloody diarrhea, and severe vomiting. Exploratory laparotomy showed 1 or more infarcted and often perforated intestinal segments in all cases. Microscopically, there was intestinal mucosal to transmural coagulative necrosis and mesenteric multifocal necrotizing eosinophilic arteritis, thrombosis, hemorrhage, and early fibroplasia. Third-stage S. lupi larvae were identified by morphologic features in 9 of 32 (28%) cases, and the species was confirmed by polymerase chain reaction in 4 cases. Nearly 50% of the dogs had been receiving prophylactic therapy, which did not prevent this form of spirocercosis.

Feline Infectious Peritonitis as a Systemic Inflammatory Disease: Contribution of Liver and Heart to the Pathogenesis.

Feline infectious peritonitis (FIP) is a fatal immune-mediated disease of cats, induced by feline coronavirus (FCoV). A combination of as yet poorly understood host and viral factors combine to cause a minority of FCoV-infected cats to develop FIP. Clinicopathological features include fever, vasculitis, and serositis, with or without effusions; all of which indicate a pro-inflammatory state with cytokine release. As a result, primary immune organs, as well as circulating leukocytes, have thus far been of most interest in previous studies to determine the likely sources of these cytokines. Results have suggested that these tissues alone may not be sufficient to induce the observed inflammation. The current study therefore focussed on the liver and heart, organs with a demonstrated ability to produce cytokines and therefore with huge potential to exacerbate inflammatory processes. The IL-12:IL-10 ratio, a marker of the immune system's inflammatory balance, was skewed towards the pro-inflammatory IL-12 in the liver of cats with FIP. Both organs were found to upregulate mRNA expression of the inflammatory triad of cytokines IL-1ß, IL-6, and TNF-α in FIP. This amplifying step may be one of the missing links in the pathogenesis of this enigmatic disease.

Infraorbital Keratin Cyst in an Umbrella Cockatoo (Cacatua alba).

A 10-year-old, female umbrella cockatoo (Cacatua alba) was presented for evaluation of a mass at the right commissure of the beak, with associated right periorbital swelling. A feather cyst was suspected, based on history and the results of a computed tomography scan and fine-needle aspirate. The cyst was surgically debrided and removed. Histopathologic results confirmed an infraorbital keratin cyst, most likely originating from a feather follicle. To our knowledge, this is the first reported case of a periorbital keratin cyst in a bird.

Feline Hypertrophic Cardiomyopathy: The Consequence of Cardiomyocyte-Initiated and Macrophage-Driven Remodeling Processes?

vHypertrophic cardiomyopathy (HCM) is the most commonly diagnosed cardiac disease in cats. The complex pathophysiology of HCM is still far from clear, but myocardial remodeling is a key process, and cardiomyocyte disarray, interstitial fibrosis, leukocyte infiltration, and vascular dysplasia are described histopathologic features. The present study systematically investigated the pathological processes in HCM, with the aim to shed more light on its pathogenesis. Hearts from 18 HCM cases and 18 cats without cardiac disease (controls) were examined, using light and transmission electron microscopy, immunohistochemistry, and morphometric approaches to identify and quantify the morphological changes. Reverse transcription-quantitative polymerase chain reaction was applied to provide additional mechanistic data on remodeling processes. In HCM, the left and right ventricular free wall and septal myocardium exhibited a significantly reduced overall cellularity, accompanied by a significant increase in interstitial Iba1-positive cells with macrophage morphology. In addition, the myocardium of almost half of the diseased hearts exhibited areas where cardiomyocytes were replaced by cell-rich fibrous tissue with abundant small and medium-sized vessels. HCM hearts also showed significantly higher transcription levels for several inflammatory and profibrotic mediators. Our findings suggest that HCM is the consequence of cardiac remodeling processes that are the result of cardiomyocyte damage and to which macrophages contribute by maintaining an inflammatory and profibrotic environment.

Age- and gender-dependent myocardial transcription patterns of cytokines and extracellular matrix remodelling enzymes in cats with non-cardiac diseases.

BACKGROUND: Age, gender and systemic diseases all influence cardiac function and remodelling. In cats, age and gender associated myocardial remodelling and the effect of systemic diseases on the myocardium have so far not been studied. The aim of the study was therefore to investigate whether relevant cytokines and extracellular matrix (ECM) remodelling enzymes are expressed in the myocardium of cats with non-cardiac diseases and whether transcription levels are influenced by age and gender. METHODS: The study was performed on myocardial samples from 26 cats aged between 2 and 19 years that had died with non-cardiac diseases. Seventeen cats were female (2 entire) and nine were male (1 entire). Of these, nine cats were diagnosed with diseases unlikely to affect the myocardium (control cats). The remaining 17 cats suffered from diseases with likely systemic effects. All hearts were assessed for any pathological changes, and the myocardium was analysed for interleukin (IL)-1, -2, -4, -6, -18, tumour necrosis factor (TNF)-α, interferon (IFN)-γ, transforming growth factor (TGF)-ß, matrix metalloproteinase (MMP)-2, -3, -13, tissue inhibitor of MMP (TIMP)-1, -2 and -3 transcriptions using quantitative RT-PCR assays. RESULTS: Despite the absence of any histological evidence of myocardial damage, inflammation and fibrosis, the myocardium of all the cats was found to constitutively transcribe cytokines and ECM remodelling enzymes, with generally higher mRNA concentrations in the atria than in the ventricles. The young and male cats exhibited higher transcription levels throughout the myocardium in comparison to the older and female cats. Furthermore, age-associated transcription pattern differed between male and female cats. CONCLUSION: The constitutive transcription of ECM remodelling enzymes suggests continuous myocardial remodelling throughout the entire life of a cat. The myocardium of young and male cats appears to be in a pro-inflammatory state, whereas in older and female cats the myocardium exhibits a reduced inflammatory reaction to systemic disease. Age-associated cardiac remodelling seems to be influenced by non-hormonal factors in male and female cats.

Equine sarcoid: In situ demonstration of matrix metalloproteinase expression.

Sarcoids are the most prevalent equine skin tumours and remain a therapeutic challenge due to their differing clinical morphology, local aggressive behaviour, and high recurrence following surgical treatment. In vitro, sarcoid derived fibroblasts are invasive and express matrix metalloproteinase (MMP) -1, -2 and -9. It was hypothesised that the MMPs produced by neoplastic cells play a role in both their local invasiveness and interaction with the overlying epidermis (picket fence formation). The objective of this morphological study was to investigate the local behaviour and in situ MMP expression pattern in sarcoids of different clinical types. A total of 43 surgically excised sarcoids were examined by histology, immunohistology for the expression of MMP-1, -2 and -9, and transmission electron microscopy. Regardless of the clinical type, sarcoids showed local invasion of the dermis and damage to the basement membrane in areas of interaction with the epidermis. This was associated with MMP-1 expression in both neoplastic cells and epidermis. The results suggest a link between MMP-1 expression and the local aggressiveness of sarcoids regardless of the clinical type.

Redescription of Hepatozoon felis (Apicomplexa: Hepatozoidae) based on phylogenetic analysis, tissue and blood form morphology, and possible transplacental transmission.

BACKGROUND: A Hepatozoon parasite was initially reported from a cat in India in 1908 and named Leucocytozoon felis domestici. Although domestic feline hepatozoonosis has since been recorded from Europe, Africa, Asia and America, its description, classification and pathogenesis have remained vague and the distinction between different species of Hepatozoon infecting domestic and wild carnivores has been unclear. The aim of this study was to carry out a survey on domestic feline hepatozoonosis and characterize it morphologically and genetically. METHODS: Hepatozoon sp. DNA was amplified by PCR from the blood of 55 of 152 (36%) surveyed cats in Israel and from all blood samples of an additional 19 cats detected as parasitemic by microscopy during routine hematologic examinations. Hepatozoon sp. forms were also characterized from tissues of naturally infected cats. RESULTS: DNA sequencing determined that all cats were infected with Hepatozoon felis except for two infected by Hepatozoon canis. A significant association (p = 0.00001) was found between outdoor access and H. felis infection. H. felis meronts containing merozoites were characterized morphologically from skeletal muscles, myocardium and lungs of H. felis PCR-positive cat tissues and development from early to mature meront was described. Distinctly-shaped gamonts were observed and measured from the blood of these H. felis infected cats. Two fetuses from H. felis PCR-positive queens were positive by PCR from fetal tissue including the lung and amniotic fluid, suggesting possible transplacental transmission. Genetic analysis indicated that H. felis DNA sequences from Israeli cats clustered together with the H. felis Spain 1 and Spain 2 sequences. These cat H. felis sequences clustered separately from the feline H. canis sequences, which grouped with Israeli and foreign dog H. canis sequences. H. felis clustered distinctly from Hepatozoon spp. of other mammals. Feline hepatozoonosis caused by H. felis is mostly sub-clinical as a high proportion of the population is infected with no apparent overt clinical manifestations. CONCLUSIONS: This study aimed to integrate new histopathologic, hematologic, clinical, epidemiological and genetic findings on feline hepatozoonosis and promote the understanding of this infection. The results indicate that feline infection is primarily caused by a morphologically and genetically distinct species, H. felis, which has predilection to infecting muscular tissues, and is highly prevalent in the cat population studied. The lack of previous comprehensively integrated data merits the redescription of this parasite elucidating its parasitological characteristics.