Detection of arenavirus in a peripheral odontogenic fibromyxoma in a red tail boa (Boa constrictor constrictor) with inclusion body disease

A captive bred red tail boa (Boa constrictor constrictor) was presented with a large intraoral mass originating from the buccal gingiva, attached to the right dentary teeth row. Based on the clinical features and histological examination, the diagnosis of a peripheral odontogenic fibromyxoma was made. Sections of liver biopsies and circulating lymphocytes contained relatively few eosinophilic intracytoplasmic inclusion bodies, indistinguishable from those observed in inclusion body disease-affected snakes. Inclusion bodies were not observed in cells comprising the neoplastic mass. Using reverse transcription polymerase chain reaction (RT-PCR), arenavirus was detected in the neoplastic tissue. Two years after surgical removal of the mass, recurrence of the neoplastic lesion was observed. Numerous large inclusion body disease inclusions were abundantly present in the neoplastic cells of the recurrent fibromyxoma. Sections of liver biopsies and circulating lymphocytes contained relatively few intracytoplasmic inclusions. The RT-PCR revealed the presence of arenavirus in blood, a liver biopsy, and neoplastic tissue. The present case describes the co-occurrence of an arenavirus infection and an odontogenic fibromyxoma in a red tail boa

Intratumoral chemotherapy in an integumentary squamous cell carcinoma in a cockatiel (Nymphicus hollandicus)

An eight-year-old, female cockatiel (Nymphicus hollandicus) was presented with anorexia, lethargy, a mass at the lower side of the wing and discoloration of the feathers. Physical examination showed an ulcerated nodular integumentary lesion of approximately 4 cm(3) ventromedial on the wing at the side of the propatagium and the humerus. Lateral and ventrodorsal radiographs revealed only hepatomegaly. After a stabilization period, surgical excision of the tumor was performed. Based on histopathological evaluation and bacterial culture of the surgically removed tissue, the lesion was typed as an integumentary squamous cell carcinoma with secondary bacterial infection (Corynebacterium sp). Four weeks postoperative, the tumor had recurred. Chemotherapeutic treatment was started with intratumoral carboplatin (1.5 mg/cm(3)) once a week. Because of further tumor growth after the second administration of carboplatin, resection of the mass was performed before the next infiltration. However, the bird died during anesthesia. Despite increase in tumor size, histopathological and immunohistochemical evaluations showed degeneration of the tumor with intercellular edema and vacuolization of the tumor cells, presumably resulting from carboplatin administration. More research is needed to investigate the efficacy and safety of the intratumoral administration of carboplatin as a treatment option in birds with integumentary squamous cell carcinoma

The Epigenetic Effects of Preconception Paternal Alcohol Exposure on Adult Health and Disease

Alcohol is a notorious teratogen and a major driver of both mental and physical defects. Recently, alcohol has been discovered to exert intergenerational effects on offspring development. While maternal exposure to alcohol in-utero has been linked to the development of fetal alcohol spectrum disorders, paternal contributions to this disorder remain poorly understood. Emerging evidence suggest the association of paternal environmental exposures and long-term metabolic dysfunction1,2. Using a mouse model, our preliminary studies have identified an association between preconception paternal alcohol use and deficits in both the prenatal and postnatal growth of the offspring. These growth defects are accompanied by altered transcriptomic profiles in the fetal liver at gestation day (GD) 14.5, which persists into the adult stages. In this study, we will examine the mechanism by which paternal alcohol exposure drives the development of prenatal growth retardation and long-term postnatal growth restriction in the offspring, as well as the abnormal metabolic response of the offspring to dietary challenge

Epigenetics and Breast Cancers

Several of the active compounds in foods, poisons, drugs, and industrial chemicals may, by epigenetic mechanisms, increase or decrease the risk of breast cancers. Enzymes that are involved in DNA methylation and histone modifications have been shown to be altered in several types of breast and other cancers resulting in abnormal patterns of methylation and/or acetylation. Hypermethylation at the CpG islands found in estrogen response element (ERE) promoters occurs in conjunction with ligand-bonded alpha subunit estrogen receptor (Erα) dimers wherein the ligand ERα dimer complex acts as a transcription factor and binds to the ERE promoter. Ligands could be 17-β-estradiol (E2), phytoestrogens, heterocyclic amines, and many other identified food additives and heavy metals. The dimer recruits DNA methyltransferases which catalyze the transfer of methyl groups from S-adenosyl-L-methionine (SAM) to 5′-cytosine on CpG islands. Other enzymes are recruited to the region by ligand-ERα dimers which activate DNA demethylases to act simultaneously to increase gene expression of protooncogenes and growth-promoting genes. Ligand-ERα dimers also recruit histone acetyltransferase to the ERE promoter region. Histone demethylases such as JMJD2B and histone methyltransferases are enzymes which demethylate lysine residues on histones H3 and/or H4. This makes the chromatin accessible for transcription factors and enzymes

Germination of Aspergillus fumigatus inside avian respiratory macrophages is associated with cytotoxicity

Although aspergillosis is one of the most common diseases in captive birds, the pathogenesis of avian aspergillosis is poorly known. We studied the role of avian respiratory macrophages as a first line of defense against avian aspergillosis. The phagocytic and killing capacities of avian respiratory macrophages were evaluated using pigeon respiratory macrophages that were inoculated with Aspergillus fumigatus conidia. On average, 25% of macrophage-associated conidia were phagocytosed after one hour. Sixteen percents of these cell-associated conidia were killed after 4 h and conidial germination was inhibited in more than 95% of the conidia. A. fumigatus conidia were shown to be cytotoxic to the macrophages. Intracellularly germinating conidia were located free in the cytoplasm of necrotic cells, as shown using transmission electron microscopy. These results suggest that avian respiratory macrophages may prevent early establishment of infection, unless the number of A. fumigatus conidia exceeds the macrophage killing capacity, leading to intracellular germination and colonization of the respiratory tract

Chytridiomycosis related mortality in a midwife toad (Alytes obstetricans) in Belgium

Chytridiomycosis, caused by the fungus Batrachochytrium dendrobatidis, contributes to amphibian declines worldwide. Recently, the fungus has shown to be widely distributed in Belgium and the Netherlands, although no clinical cases of the disease have been diagnosed yet. This case report describes the first case of mortality due to chytridiomycosis in Belgium in a wild population of midwife toads (Alytes obstetricans). The presence of clinical chytridiomycosis, combined with the relatively high prevalence of the fungus in Belgium, emphasizes the urgent need for a thorough study on the impact of infection on the native amphibian populations in Belgium