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Results for “Steatitis”

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At least 55 records · Page 3Linked to original sources
PubMed2004

A sequential study of pathological findings in Atlantic halibut, Hippoglossus hippoglossus (L), throughout one year after an acute outbreak of viral encephalopathy and retinopathy.

Following a natural outbreak of viral encephalopathy and retinopathy (VER) at a commercial farm in Norway, surviving Atlantic halibut, Hippoglossus hippoglossus, were sequentially studied for distribution of nodavirus, immune response and histopathology over 1 year. Typical clinical signs and histopathology of VER were observed during the acute stage of the disease. Most of the surviving fish became subclinical carriers of nodavirus with clusters of nodavirus-containing cells in the central nervous system. Four random samplings of presumably healthy fish were performed from two fish groups, with low and high growth rates respectively, over a 7-month period. Immunohistochemical (IHC) examination revealed a higher number of nodavirus-positive cells in fish with a low growth rate than in fish with a high growth rate. All IHC positive fish were also reverse transcriptase polymerase chain reaction (RT-PCR) positive for nodavirus and for nodavirus antibodies detected by enzyme-linked immunosorbent assay (ELISA) at all sampling points. The percentage of PCR- and ELISA-positive fish remained high throughout the year, while the number of IHC-positive fish decreased, especially in the group with a high growth rate. Several other histopathological changes were observed, including pericarditis, steatitis, changes in liver and kidney, and necrosis of the intestinal wall. None of these findings seemed to be related to the nodavirus infection. Nodavirus was reisolated in cell culture from subclinically infected fish one year after the acute VER outbreak, which indicates that the virus was still infectious.

Animals↗
PubMedDate not supplied

Sclerosing encapsulating peritonitis in four dogs and a cat.

Sclerosing encapsulating peritonitis (SEP) was diagnosed in four dogs and one cat. Clinical signs included vomiting, abdominal pain, palpable abdominal mass, and ascites. The abdominal fluid was red-tinged and contained large numbers of red blood cells, macrophages, mixed inflammatory cells, reactive mesothelial cells, and fibroblasts. At surgery, the typical appearance was of multiple surfaces covered with granulation tissue or fibrous tissue or both. Multiple adhesions were often present. Causes of SEP included steatitis, fiberglass ingestion, and bacterial infection. Treatment included administration of antibiotic, corticosteroid, and diuretic medications. The major long-term management problems were chronic weight loss, ascites, and progression of concurrent disease.

Animals↗
PubMed1995

Diseases in young farmed crocodiles in Irian Jaya.

Thirty-eight young crocodiles that were emaciated and were euthanased or were found dead on 12 farms in Irian Jaya were examined post mortem. Major diseases were coccidiosis (nine crocodiles), pentastomiasis (four), visceral gout (two) and bacterial pneumonia and septicaemia (two). Other diseases and infections were steatitis, fungal pneumonia, gastric capillariasis, haemogregarine infection, ascariasis, filarioid infection and the presence of flukes in the intestine, kidney and blood. Multiple parasitism due to the collection of hatchlings in the wild was considered the primary cause of the ill-thrift and death of the crocodiles.

Alligators and Crocodiles↗
PubMed2002

Chronic nodular panniculitis in a three-year-old mare.

The clinical signs of chronic nodular panniculitis in a three-year-old mare were consistent with a diagnosis of sterile nodular panniculitis, but the mare had histopathological signs of both generalised steatitis and sterile nodular panniculitis. The mare was deficient in vitamin E and selenium.

Animals↗
PubMed2006

Panniculitis in a horse with peripancreatitis and pancreatic fibrosis.

A 22-year-old pinto mixed breed mare was admitted for evaluation of severe colic signs and gastric reflux. Multiple nonpainful, variably sized hard masses were palpated in the subcutis over the thorax, abdomen, and hindquarters of the horse. The mare was diagnosed with sterile peritonitis and had systemically high gamma-glutamyltransferase, amylase, and lipase. Three days into treatment she became febrile with signs of persistent and mild abdominal discomfort; euthanasia was elected. Necropsy revealed peripancreatitis, pancreatic fibrosis, abdominal steatitis and panniculitis. Panniculitis associated with peripancreatitis has been described in humans and dogs but not in horses. Pathogenic models for this entity are discussed.

Animals↗
PubMed2003

A third report of "golf ball disease" in an Amazon River dolphin (Inia geoffrensis) associated with Streptococcus iniae.

An Amazon River dolphin (Inia geoffrensis) developed a dermatologic syndrome characterized by the occurrence of slow-growing, nodular, s.c. abscesses. Initial biopsies, cultures, and cytologic analysis of needle aspirates from the abscesses indicated steatitis with probable secondary, gram-negative bacterial infection. Treatment with dietary vitamin E supplement and broad-spectrum antibiotics yielded minimal improvement. Subsequent cultures revealed Streptococcus iniae in addition to several gram-negative bacteria. Vigorous surgical management of the abscesses, including lancing, debridement, and irrigation, combined with antimicrobial therapy specific for Streptococcus and gram-negative organisms, and improvement of the animal's diet and environmental water quality led to gradual recovery. When the animal was ill, it demonstrated an inflammatory leukogram and transient uremia. Streptococcus iniae is a serious pathogen of aquacultured fishes and humans and should be included in the differential diagnosis of chronic dermatopathy in river dolphins. Specific antimicrobial therapy, excellent water quality, surgical management of abscesses, and adherence to sanitary protocols should be observed in cases of suspected S. iniae infection in dolphins.

Abscess↗
PubMed1988

Pancreatic abscess in dogs: six cases (1978-1986).

Pancreatic abscess was diagnosed by exploratory celiotomy in 6 dogs. The most common clinical signs included acute onset of lethargy (n = 5), anorexia (n = 6), vomiting (n = 5), and diarrhea (n = 2). Physical examination revealed pain response to abdominal palpation (n = 5), depression (n = 5), icterus (n = 3), fever (n = 3), and cranial abdominal mass (n = 2). Consistent preoperative clinicopathologic abnormalities included leukocytosis with left shift, observance of toxic neutrophils on the blood smear, hyperlipasemia, hyperamylasemia, hyperbilirubinemia, and increased serum alkaline phosphatase activity. In 5 of 6 dogs, abdominal radiography revealed increased soft tissue density in the cranial portion of the abdomen. Ultrasonography performed on 4 dogs confirmed pancreatic mass. In all dogs, exploratory celiotomy revealed a cavitary pancreatic mass that contained sterile, mucopurulent material. Histopathologic diagnoses included acute necrotizing or chronic-active pancreatitis and steatitis. Two dogs were euthanatized at the time of diagnosis, and the remaining 4 were treated by use of pancreatic debridement(s), open abdominal drainage, and intensive administration of fluids and antibiotics. One dog was euthanatized 4 days after surgery, because of progressive pancreatic abscessation. Three dogs recovered and were discharged.

Abscess↗
PubMed1994

[Simulation of an extrauterine pregnancy by a fatty tissue tumor in a Galloway cow].

In an eight-year old Galloway cow, an ectopic pregnancy with mummification of the fetus which had been assumed because of history and clinical examination of the animal was diagnosed as a "tumor of the adipose tissue" (steatitis) following exploratory laparotomy. Possible problems of obesity in cows of extensively kept breeds are discussed.

Animals↗
PubMedDate not supplied

Valproate-induced hepatic steatogenesis in rats.

The administration of high-dose valproic acid (VPA) (750 mg per kg) consistently produced significant microvesicular steatosis in mature Sprague-Dawley rats after 48 hr. Similar changes occurred in animals pretreated with phenobarbital which received a lower dose of VPA (350 mg per kg), but no steatosis was seen in animals treated with the low-dose VPA alone. The steatogenic effect of VPA is most likely mediated by a toxic metabolite. It can also be speculated that phenobarbital, by enhancing the inducing effects of the hepatic mixed-function oxidase system, may lead to increased conversion of VPA to a toxic metabolite. Young and weanling rats appeared to be resistant to the steatogenic effects of VPA. Reproduction of microvesicular steatosis in this experimental; model may permit exploration of factors that enhance or inhibit VPA-induced hepatic injury.

Animals↗
PubMed2006

Pansteatitis and severe hypocalcaemia in a cat.

A 13-year-old Siamese cat was presented for investigation of lethargy and progressive abdominal enlargement. Serum chemistry revealed severe reduction of total and ionised serum calcium. The omentum appeared hyperechoic with scattered hypoechoic foci on abdominal ultrasound examination. Elevated serum parathormone and low fractional excretion of calcium excluded a parathyroid disorder and renal loss of the electrolyte. During laparotomy the omentum appeared opaque, white and firm. Post-mortem examination revealed that the thoracic and subcutaneous fat was also affected. Histopathology confirmed the diagnosis of pansteatitis with diffuse calcium soaps formation. While, severe hypocalcaemia is occasionally seen in cats, the association with pansteatitis has not been reported previously. In man, a cause-and-effect relationship between calcium soaps and hypocalcaemia is recognised, though the association is rare.

Adipose Tissue↗
PubMed1999

Aflatoxin B1-induced hepatic steatosis: role of carbonyl compounds and active diols on steatogenesis.

Aflatoxin B1 (AFB1) exerts a chronic carcinogenic and an acute toxic effect on animals. Whereas the mechanism for carcinogenicity is known, no mechanism has been proposed for the toxic action. Among the most prominent signs of aflatoxicosis in several species, including birds and mammals, are hypolipidaemia, hypocholesterolaemia, and hypocarotenaemia, associated with severe hepatic steatosis and weight loss. We suggest that these signs of acute imbalance of lipid metabolism can be the result of the chemical modification (blocking) of key lysyl residues on the LDL protein B-100 by the activated AFB1 molecule. Modified LDLs are not recognised by their specific receptors and thus are rejected by peripheral cells. Upon return to the liver, the modified particles bind to the sinusoidal lining cells. Lipid starvation of peripheral tissues takes place while fat accumulates in the liver. This abnormal state is maintained and reinforced by further modification of nascent apoproteins, which in turn become unable to receive a lipid load for as long as aflatoxin continues to be available in the liver.

Aflatoxin B1↗
PubMed2003

Feline pansteatitis revisited: hazards of unbalanced home-made diets.

Pansteatitis is caused by the consumption of high levels of unsaturated fatty acids and/or the insufficient intake of vitamin E, leading to inflammation of adipose tissue. This disease has been related to fish-based diets. However, non-conventional diets must also be considered. The authors present case records of two cats with pansteatitis, for which diet consisted mostly of pig's brain, comparing them with eight cases of disease in cats eating mainly oily fish. Cats fed pig's brain did not show clinical signs, while cats eating oily fish presented inappetence, depression, reluctance to move and subcutaneous nodules painful on palpation. Cats eating pig's brain did not show any change in blood parameters, while cats fed oily fish presented leukocytosis and anaemia. Histological examination confirmed pansteatitis in all cats, independently of the diet. All animals except one of the cats eating oily fish recovered after medical treatment and change of the feeding regime.

Animals↗
PubMed2004

The ins and outs of mitochondrial dysfunction in NASH.

Rich diet and lack of exercise are causing a surge in obesity, insulin resistance and steatosis, which can evolve into steatohepatitis. Steatosis and nonalcoholic steatohepatitis (NASH) can also be induced by drugs such as amiodarone, tamoxifen and some antiretroviral drugs. There is growing evidence that mitochondrial dysfunction, and more specifically respiratory chain deficiency, plays a role in the pathophysiology of NASH whatever its initial cause. In contrast, the B-oxidation of fatty acids can be either increased (as in insulin resistance-associated NASH) or decreased (as in drug-induced NASH). However, in both circumstances, the generation of reactive oxygen species (ROS) by the damaged respiratory chain is augmented, as components of this chain are over-reduced by electrons, which then abnormally react with oxygen to form increased amounts of ROS. Concomitantly, ROS oxidize fat deposits to release lipid peroxidation products that have detrimental effects on hepatocytes and other hepatic cells. In hepatocytes, ROS and lipid peroxidation products further impair the respiratory chain, either directly or indirectly through oxidative damage to the mitochondrial genome. This, in turn, leads to the generation of more ROS and a vicious cycle ensues. Mitochondrial dysfunction can also lead to apoptosis or necrosis depending on the energy status of the cell. ROS and lipid peroxidation products also activate stellate cells, thus resulting in fibrosis. Finally, ROS and lipid peroxidation increase the generation of several cytokines (TNF-alpha, TGF-B, Fas ligand) that play sundry roles in the pathogenesis of NASH. Recent investigations have shown that some genetic polymorphisms can significantly increase the risk of steatohepatitis and that several drugs can prevent or even reverse NASH. For the next decade, reducing the incidence of NASH will be a major challenge for hepatologists.

Animals↗
PubMed2002

P-selectin glycoprotein ligand-1 (rPSGL-Ig)-mediated blockade of CD62 selectin molecules protects rat steatotic liver grafts from ischemia/reperfusion injury.

We examined the effects of early blockade of CD62 selectin-mediated adhesive interactions in steatotic rat liver models of ex vivo cold ischemia followed by reperfusion or transplantation by administration of P-selectin glycoprotein ligand-1 (rPSGL-Ig). In the model of cold ischemia/reperfusion, livers pretreated ex vivo with rPSGL-Ig at harvesting from obese Zucker rats showed significantly decreased portal resistance, increased bile production, and diminished hepatic endothelial neutrophil infiltration, as compared with untreated controls. Pretreatment of fatty livers with rPSGL-Ig prior to transplantation extended the survival of lean Zucker rat recipients from 40% to 90%. This effect correlated with significantly improved liver function, depressed neutrophil activity, and decreased histologic features of hepatocyte injury. Intragraft expression of CD62 P-selectin was similar in both recipient groups. rPSGL-Ig treatment decreased intragraft infiltration by CD3/CD25 cells, diminished expression of pro-inflammatory TNFalpha, IL-6, iNOS, IL-2 and IFN-gamma, without significantly affecting mRNA levels coding for anti-inflammatory IL-4. Thus, rPSGL-Ig blockade of CD62-mediated adhesive interactions protects against severe ischemia/reperfusion injury suffered otherwise by steatotic rat livers. These findings document the potential utility of rPSGL-Ig in increasing the transplant donor pool through modulation of marginal steatotic livers.

Animals↗