Acquired Skin Fragility Syndrome and Diabetes Mellitus Secondary to Hyperadrenocorticism in a Cat

Background: Acquired skin fragility syndrome is a rare disorder which affects adult to senior cats with no history of skin trauma. Acquired skin fragility syndrome and diabetes mellitus, unlike the dog, are highly associated to feline hyperadrenocorticism (HAC) and, often, undiagnosed, what may accentuate the skin lesions and cause management complications. This report aimed to describe a case of acquired skin fragility syndrome and diabetes mellitus secondary to spontaneoushyperadrenocorticism in a cat, focusing on the chronic dermatological signs and their management, as well as on the treatment of the primary disease.Case: An approximately 7 year-old male mixed breed feline was admitted to the University Veterinary Hospital of an Institution with a history of polyphagia, polyuria and polydipsia, and skin ulcers on the trunk and in the cervical region about 2 months after onset and difficult to heal. Laboratory examinations indicated leukocytosis with lymphopenia, decreased urine specific gravity, glycosuria and hyperglycemia. The fasting plasma glucose level, the dexamethasone suppression test and the bilateral adrenal gland enlargement, visualized by ultrasonography, revealed diabetes mellitus and spontaneous hyperadrenocorticism, respectively. Histological skin findings indicated feline acquired skin fragility syndrome. Skin wound treatment through cleaning, protection and antibiotic therapy, and administration of insulin and trilostane were performed. After 6 months of trilostane therapy, adrenocorticotropic hormone (ACTH) stimulation test was performed, which demonstratednormal cortisol values 4 h after administration, which allowed maintenance of the dosage. After 12 months of the diagnosis of skin fragility syndrome and diabetes mellitus secondary to HAC, the patient did not present new skin lesions, fasting glycemia was within the reference values without insulin therapy and maintained only the prescription of trilostane.Discussion: The pituitary-dependent hyperadrenocorticism was the cause of the skin fragility syndrome, and it could be confirmed by the dexamethasone suppression test and the ultrasonography, which demonstrated bilateral adrenal gland enlargement. Healing of the wounds caused by the acquired skin fragility syndrome as well as the absence of new lesions may occur if the primary cause is found and treated adequately. Signs of polyuria, polydipsia and polyphagia verified inthe patient of this report are nonspecific and allow the suspicion of both diabetes mellitus and hyperadrenocorticism. The return of glycemia to basal levels and the interruption of insulin demonstrated that diabetes mellitus was transient and secondary to hyperadrenocorticism. Therefore, it is indicated in situations similar to the clinical condition described in thepatient of this report, to perform tests for diabetes mellitus and HAC. Trilostane can reduce the clinical signs of hyperadrenocorticism, but sometimes maintenance of insulin therapy is needed. The use of the drug improved the skin lesions in the cat of the current report and also allowed for the interruption of insulin administration. Those skin lesions which areof spontaneous occurrence and persistent, with no previous history of trauma and that do not respond to treatment, may alert clinicians to investigate underlying causes of non-dermatological origin and guide owners through the likely slow skin lesions healing until diagnosis and adequate therapeutic response of the primary disease.Keywords: Cushing disease, feline, skin, trilostane, wound healing

Acquired Diaphragmatic Eventration in a Dog

Background: Diaphragmatic eventration is characterized by weakness of the diaphragmatic muscle, which leads to cranial dislocation of the affected diaphragm and, ultimately, in dyspnea. This condition is rare in humans and even rarer in animals, and may be congenital or acquired. The acquired form is less commom and may be induced by trauma or inflammation and neoplastic invasion of the phrenic nerve. Here, we report a case of acquired diaphragmatic eventration in a dog, with the aim of increasing the knowledge of this condition in animals and helping others to recognize and treat future cases.Case: A 12-year-old male dachshund presented with severe dyspnea, exercise intolerance and episodes of coughing. Based on a physical examination and imaging, the main suspicion was a diaphragmatic hernia, and surgery was performed. When the surgeon entered the thoracic cavity, an extremely thin - yet, intact - right hemidiaphragm was observed. The left side of the diaphragm was normal. A polypropylene mesh was sutured to the affected diaphragm in an attempt to strengthen the hemidiaphragmatic muscles and prevent further insinuations of viscera into the thoracic cavity. The dog developed bronchopneumonia, postoperatively, and was hospitalized and treated with antibiotics, analgesics and support medication. However, the dog died five days after surgery. A postmortem examination revealed that the right side of the diaphragm was markedly thin and flaccid. Diaphragm samples were collected for histopathological examination. For comparison, a sample of normal diaphragm was collected from a same age, matched dachshund that died due to an unrelated condition. This tissue was called “diaphragm control”, and it was collected in order to compare the histologic features of a normal diaphragm muscle with the affected one. Histopathology revealed a marked reduction of muscle fibers. In the affected sample, replacement of these fibers by fibrous connective tissue and a marked infiltration of fat were seen among the remaining muscle fibers.  Multifocal areas of necrosis were also observed affecting some muscles fibers. Microscopic comparisons of both diaphragm samples (affected vs. control) revealed a drastic difference in the amount of muscle fibers and fat, corroborating the intense diaphragmatic atrophy observed in the diaphragm from the affected dog. Based on clinical presentation, the gross lesions observed during surgery and later during the post mortem examination, and histopathological findings, a definitive diagnosis of acquired diaphragmatic eventration was established.Discussion: Diaphragmatic eventration is rarely reported in small animal clinics and thus may be confused with other conditions. It must be mainly differentiated from diaphragmatic hernia and should be considered as a differential diagnosis when an animal, regardless of age, presents with dyspnea, apathy and coughing episodes.  On suspecting diaphragmatic eventration, surgical intervention should be carried out as soon as possible. The recommended treatment is plication of the affected hemidiaphragm. However, in the present case, a polypropylene mesh was sutured to the affected area to support the atrophic muscles. It is thought that, trauma injured the dog’s phrenic nerve, affecting right hemidiaphragmatic innervation, and generating progressive atrophy of diaphragmatic muscle fibers. Subsequently, the dog developed diaphragmatic eventration due to diaphragmatic fragility. Diaphragmatic eventration is a very rare disorder in small animals and can be difficult to diagnose based solely on physical and radiographic examinations

Melanocytoma-acanthoma in a Dog

Background: Melanocytic neoplasms are skin tumors that often occur in dogs.  However, melanocytoma-acanthoma, also called melanoacanthoma, is a benign melanocytic neoplasm rarely reported in this species, which has been described only three times in the veterinary literature. Briefly, this tumor is characterized by a single, painless, darkly pigmented and firm cutaneous papule or nodule. Histologically, it is composed of mixed populations of well-differentiated melanocytes and keratinocytes, unlike traditional melanocytic tumors (melanoma and melanocytoma). These cells are arranged in lobules surrounded by collagenous stroma. Melanocytes are large epithelioid cells containing varying amounts of melanin. Keratinocytes form anastomosing trabeculae with peripheral palisading, and small cysts containing amorphous or laminated keratin. The definitive diagnosis of melanocytoma-acanthoma is based on histopathological findings. This report describes a case of melanocytoma-acanthoma in a dog in Brazil.Case: A 9-year-old female miniature Schnauzer dog was examined at the Veterinary Hospital of the Federal University of Santa Maria, where a single, firm, pigmented papule was found in the auricle. The lesion had started 15 days earlier. Hematological tests and serum biochemistry profile were normal. An excisional biopsy of the papule was surgically removed and subjected to histopathological examination. The tissue was fixed in 10% neutral buffered formalin, processed routinely and embedded in paraffin wax. Sections were stained with hematoxylin and eosin (HE). A histopathological examination revealed a nonencapsulated, well-defined, extensive, densely cellular proliferation located in dermis. This proliferation was composed of lobules and nests of well-differentiated stratified squamous epithelium closely associated with neoplastic melanocytes, surrounded by thin bundles of fibrous stroma. A diagnosis of melanocytoma-acanthoma was established based on these histological features.Discussion: The first description of melanocytoma-acanthoma in humans was as melano-epithelioma, classified into subtypes I and II. Both subtypes are benign neoplasms composed of well-differentiated melanocytes and keratinocytes, which are distinguished from one another based on the amount and distribution of melanocytes. Type I melano-epithelioma is characterized by proliferative lobules of melanocytes and keratinocytes, including melanocytes scattered diffusely among keratinocytes. Type II melano-epithelioma involves only the proliferation of keratinocytes, while melanocytes are limited to the basal layer of keratinocyte lobules. To clarify this condition, some authors use the term “melanoacanthoma” to indicate the above-described type I melano-epithelioma, and seborrheic keratosis to indicate type II melano-epithelioma. However, other authors use the term melanoacanthoma to denote the two conditions (types I and II melano-epithelioma). On the other hand, veterinary medicine does not recognize subtypes, instead using the term melanocytoma-acanthoma, and more recently, melanoacanthoma, to denote this cutaneous neoplasm. Melanocytoma-acanthoma in dogs was first reported in Spain, and involved a 2-year-old German shepherd dog. Later, two other cases were described in adult mixed-breed dogs, one in South Korea and the other in Libya. This is the first report of melanocytoma-acanthoma in a dog in Brazil. The gross and histopathological appearance of this case matches that described in the previous cases (a single, well-defined, pigmented cutaneous papule or nodule). Histologically, the differential diagnosis for melanocytoma-acanthoma includes melanoma, melanocytoma, trichoepithelioma, and sebaceous epithelioma.

CARACTERÍSTICAS FÍSICO-QUÍMICAS E CITOLÓGICAS DO LÍQUIDO SINOVIAL DE PÔNEIS COM MODELO DE SINOVITE INDUZIDA

O objetivo deste estudo foi descrever as principais alterações do líquido sinovial de seis pôneis com sinovite induzida através da administração intra-articular de 0,5 mL de adjuvante completo de Freund. As características físico-químicas e citológicas foram avaliadas antes da indução da sinovite (T0), cinco dias pós-indução (T1) e, a partir daí, às 12 (T2), 24 (T3), 48 (T4), 72 (T5), 96 (T6) e 120 horas (T7). A articulação contralateral sadia serviu como controle. A proteína, a viscosidade e a qualidade da precipitação da mucina não diferiram (P>0,05) entre as articulações em T0. Em T1, o líquido sinovial das articulações com sinovite apresentou aumento da concentração de proteína (6,5 g/dl), baixa viscosidade e baixa qualidade do precipitado da mucina, resultados que permaneceram estáveis até T7. Nas articulações sadias não foi observada diferença na viscosidade e qualidade da mucina até o final do experimento, mas, devido às artrocenteses, a proteína aumentou (

Surto de febre amarela em bugios

A febre amarela é uma infecção aguda causada por um Flavivirus (VFA) transmitido por mosquitos, endemica nas regiões tropicais da América do Sul. O objetivo desta nota prévia é relatar a ocorrência de um surto da doença no Sul do Brasil. Durante os meses de outono de 2001, um surto de doença em bugios vitimou aproximadamente oitenta exemplares da espécie Alouatta fusca numa floresta no Oeste do Rio Grande do Sul (Santo Antônio das Missões e Garruchos). Os habitantes do lugar relataram que os animais caiam das árvores gravemente enfermos ou mortos. Os populares observaram que os animais tinham amarelamento acentuado da pele e mucosas visíveis. O cadáver de um dos bugios encontrados mortos foi necropsiado no Laboratório de Patologia Veterinária do Hospital Veterinário da Universidade Federal de Santa Maria. O animal era uma fêmea em mau estado corporal e as lesões observadas na necropsia consistiam em icterícia acentuada de mucosas, grandes vasos e órgãos internos. A bexiga continha urina amarelada com flocos esbranquiçados. Tecidos de vários órgãos foram incluídos em parafina e corados pela hematoxilina e eosina. Foi detectada necrose de coagulação massiva do fígado com degeneração gordurosa dos hepatócitos remanescentes, degeneração do epitélio tubular renal com cilindros hialinos na luz tubular, e necrose variável dos folículos linfóides do baço. As lesões foram sugestivas de febre amarela. Foi realizada imunoistoquímica de cortes histológicos de fígado e rim para detecção de antígenos do vírus da febre amarela (VFA). Foi usado um anticorpo policlonal de camundongo (diluição 1:1600) e um complexo comercial estreptadividina-fosfatase alcalina que reagiu com a biotina ligada ao anticorpo secundário. O teste foi positivo para antígenos do VFA e o diagnóstico de febre amarela em primatas foi formulado pela primeira vez no Estado do Rio Grande do Sul

Doenças de bovinos no Sul do Brasil: 6.706 casos

As doenças que acometem bovinos na região Sul do Brasil foram analisadas através de um estudo dos protocolos de necropsia de 6.706 bovinos examinados pelo Laboratório de Patologia Veterinária da Universidade Federal de Santa (LPV-UFSM), Rio Grande do Sul, de 1964-2008. Desses, 20,9% foram necropsias realizadas no LPV-UFSM e 79,1% foram amostras de tecidos submetidos por veterinários de campo. Dos 6.706 exames, 62,9% tinham diagnóstico conclusivo. A autólise ou material insuficiente foram as principais razões para a ocorrência de casos com diagnóstico inconclusivo. A intoxicação por Senecio spp. foi a principal causa de morte de bovinos neste estudo. As plantas tóxicas e as toxiinfecções juntas, responderam por 22,8% dos casos com diagnóstico conclusivo. As doenças inflamatórias e as parasitoses juntas contribuíram com mais de 30% das doenças de bovinos e a tristeza parasitária bovina foi a principal doença nessa categoria. As demais categorias distribuíram-se na seguinte ordem: neoplasmas e lesões tumoriformes (13,87%), doenças causadas por agentes físicos (2,7%), doenças metabólicas e nutricionais (2,46%), distúrbios circulatórios (1,4%), doenças degenerativas (1,1%), distúrbios do desenvolvimento (0,54%), distúrbios iatrogênicos (0,16%), distúrbios imunogênicos (0,19%) e, outros distúrbios (0,21%). A alta prevalência de tumores em bovinos foi atribuída a ingestão crônica de Pteridium aquilinum, uma toxicose comum na região. As principais doenças de bovinos na região estudada estão relacionadas a fatores ambientais resultante do manejo característico de criação predominantemente extensiva adotado na região.The diseases affecting cattle in southern Brazil were studied through a review of the necropsy reports filed at the Laboratório de Patologia Veterinária of the Universidade Federal de Santa Maria (LPV-UFSM), Rio Grande do Sul, and pertaining to the examination of 6.076 cattle during 1964-2008. Of those exams 29.9% were necropsies performed at the LPV-UFSM and 79.1% were mailed-in organ fragments from necropsies performed at the field by veterinary practitioners. Autolysis and non-representative sampling o mailed in organs were the main reasons for non-conclusive diagnosis. Poisoning by Senecio spp. was the main cause of death in cattle in this study and poisonous plants together with toxi-infections accounted for 22.8% of the cases with conclusive diagnosis. Inflammatory diseases together with parasitic diseases accounted for more than 30% of cattle diseases and babesiosis and anaplasmosis were the main diseases in this category. Other categories were distributed in the following order: neoplasms and tumor-like lesions (13.87%), diseases caused by physical agents (2.7%), metabolic and nutritional diseases (2.46%), circulatory disturbances (1.4%), degenerative diseases (1.1%), developmental disorders (0.54%), iatrogenic diseases and sundry lesions. The high prevalence of tumors in cattle in this study was attributed to the chronic ingestion of Pteridium aquilinum, a common toxicosis in the region. The main diseases in cattle from the studied region are related to environmental factors associated to the predominantly husbandry practices adopted in the region