Infectious bursal disease is a highly contagious disease of young chickens caused by Infectious bursal disease virus (IBDV). Genome segment A encodes the capsid protein (VP2), while segment B encodes the RNA-dependent RNA polymerase (VP1). In the present study, we trace the molecular epidemiology of IBDV in Brazil by analyzing 29 isolates collected in the major regions of poultry production. To genetically characterize the isolates, phylogenetic and population dynamic analyses were conducted using 68 VP1 (2634 nt) and 102 VP2 (1356 nt) coding sequences from IBDV isolates from different regions of the world. Furthermore, the evolution of IBDV was analyzed by characterizing the selective forces that operated during the diversification of viral isolates. We show that IBDV isolates were introduced into Brazil mainly from the Netherlands and the USA. These introductions were associated with all Brazilian poultry production regions analyzed in this work. In addition, we show that the evolution of IBDV has been shaped by a combination of very low recombination rates and relatively high rates of nucleotide substitution (2.988×10(-4) for VP1 and 3.2937×10(-4) for VP2), which themselves are a function of purifying selection operating on VP1 and VP2. Furthermore, our extended Bayesian skyline plot suggests that the increase in the effective population size of isolates of IBDV is consistent with its epidemiological history, with a large increase during the emergence of acute outbreaks of IBD in the 1980s.

Feline coronavirus (FCoV) is an enveloped single-stranded RNA virus, of the family Coronaviridae and the order Nidovirales. FCoV is an important pathogen of wild and domestic cats and can cause a mild or apparently symptomless enteric infection, especially in kittens. FCoV is also associated with a lethal, systemic disease known as feline infectious peritonitis (FIP). Although the precise cause of FIP pathogenesis remains unclear, some hypotheses have been suggested. In this review we present results from different FCoV studies and attempt to elucidate existing theories on the pathogenesis of FCoV infection.

The Feline coronavirus (FCoV) can lead to Feline infectious peritonitis (FIP), which the precise cause is still unknown. The theory of internal mutation suggests that a less virulent biotype of FCoV (FECV) would lead to another more pathogenic biotype (FIPV) capable of causing FIP. In this work, the 7b gene was amplified from 51 domestic cat plasma samples by semi-nested PCR and tested through phylogenetic and phylogeographical approaches. The 7b gene of Brazilian isolates displayed high conservation, a strong correlation between the geographic origin of the viral isolates and their genealogy, and its evolution was possibly shaped by a combination of high rates of nucleotide substitution and purifying selection.

The aim of this article is to describe a case of adrenocortical neoplasm with manifestation of hyperadrenocorticism. Adrenocortical tumors originate from different types of cells and present varied clinical manifestations, which can be functional or non-functional. Adenocarcinomas are autonomous and functional in most cases, leading to excessive secretion of glucocorticoids, regardless of pituitary control. They corroborate the occurrence of hyperadrenocorticism (HAC) due to interference in the synthesis of cortisol. Clinical signs can be observed, as polyuria, compensatory polydipsia, polyphagia, blood pressure alterations, cardiac, renal and endocrine dysfunctions, among others. Diagnosis can be made in various ways, such as urinary cortisol measurements, adrenocorticotropic hormone stimulation, low-dose dexamethasone suppression tests, and imaging tests and histopathology. This article reports the case of a 13-year-old mixed-breed female dog with signs of polyuria and polydpsia. After discarding the initial diagnoses (diabetes mellitus and/or renal alterations), HAC was suspected, with further tests being performed. The test results showed an increase in the adrenal region, and adrenalectomy and hormone replacement with trilostane were recommended. The diagnosis of HAC was confirmed by histopathology as HAC secondary to adrenal gland adenocarcinoma. The patient also developed diabetes mellitus during postoperative treatment with prednisone, which made it necessary to discontinue the medication.