Treatment of a strandling whale (Kogia breviceps)

A stranded young pygmy sperm whale was nursed for four days in a pool, fed an artificial diet via a stomach tube and injected intramuscularly with antibiotics and corticosteroids. Initially unable to maintain her balance or to swim, she showed progressive improvement and by the third day could swim and dive quite strongly. Early on the fifth day her condition rapidly worsened and she died. An autopsy revealed extensive deep bruising in the head and mid-abdominal regions consistent with injuries sustained during the stranding.     

Microbial diversity and structure in the gastrointestinal tracts of two stranded short-finned pilot whales (Globicephala macrorhynchus) and a pygmy sperm whale (Kogia breviceps)

Information on the gut microbiome composition of different mammals could provide novel insights into the evolution of mammals and succession of microbial communities in different hosts. However, there is limited information on the gut microbiome composition of marine mammals, especially cetaceans because of sampling constraints. In this study, we investigated the diversity and composition of microbial communities in the stomach, midgut, and hindgut of 2 stranded short-finned pilot whales (Globicephala macrorhynchus) and hindgut of a stranded pygmy sperm whale (Kogia breviceps) by using 16S rRNA gene amplicon sequencing technology. On the basis of the 50 most abundant operational taxonomic units, principal coordinate analysis, and non-metric multidimensional scaling analysis, we confirmed that the gut microbial communities of the 3 whales were different. Our results revealed that the gut microbiome of 1 stranded short-finned pilot whale GM16 was dominated by Firmicutes (mainly Clostridium) and Fusobacteria; whereas that of the other pilot whale GM19 was composed of Gammaproteobacteria and Bacteroidetes (mainly Vibrio and Bacteroides, respectively), probably caused by intestinal disease and antibiotic treatment. The gut microbiome of the pygmy sperm whale was dominated by Firmicutes and Bacteroidetes. Moreover, different gastrointestinal tract regions harbored different microbial community structures. To our knowledge, this is the first report of the gut microbiome of short-finned pilot whales, and our findings will expand our current knowledge on microbial diversity and composition in the gastrointestinal tract of cetaceans.     

Cardiomyopathy in stranded pygmy and dwarf sperm whales

Necropsy and histologic examinations were performed in 23 pygmy sperm whales (Kogia breviceps) and 6 dwarf sperm whales (Kogia simus) that had been stranded singly or in cow-calf pairs along the southeastern coastline of the United States. At necropsy, the gross findings in the adult whales included pale, flabby right ventricles. Microscopically, lesions in the hearts of the whales were characterized by moderate to extensive myocellular degeneration, atrophy, and fibrosis. Similar changes were not seen in 5 of 6 sexually immature whales or in the whale calves. Hepatic changes were consistent with heart failure. The cause of the myocardial lesions was not determined. The systemic effects of failing myocardium probably were a major reason for the stranding of the adult whales.     

Subacute toxicity of dietary 3-acetyldeoxynivalenol in mice.

3-Acetyldeoxynivalenol was incorporated into a semisynthetic diet at levels of 2.5, 5, 10 or 20 ppm and fed to mice for up to 48 days. Body weights and feed consumption were determined, and blood samples for hematological evaluation were taken. Selected tissues were examined microscopically and the humoral immune response was assessed using the Jerne plaque assay. 3-Acetyldeoxynivalenol caused a dose-related depressed feed consumption within the first seven days and reduced body weight until day 14 when fed at levels up to 10 ppm. When fed at a level of 20 ppm, an initial depression in body weight gain and a general malaise were followed by a return to normal. At necropsy, no macroscopic or microscopic lesions could be found. The immune response was not significantly affected after seven or 14 days, but at 21 days, a dose-dependent enhanced response was observed. The findings indicate that, after an initial period of reduced feed intake, animals are apparently able to overcome the toxic effects of 3-acetyldeoxynivalenol.     

Subacute toxicity testing of ochratoxin A and citrinin in swine.

Fourteen pigs were fed ochratoxin A and citrinin through a stomach tube at daily doses of 0.02 and 0.01 mg/kg body mass for 57 days. These toxin doses correspond to the average toxin contamination level of feeds in Central Europe. The clinical status of the pigs was monitored and clinical laboratory, haematological and mycotoxin-analytical examinations were performed throughout the trial. At the end of the experiment gross and histopathological examinations were carried out. The results of ochratoxin A and citrinin determination in the blood, obtained by high-performance liquid chromatography (HPLC), are important from the food hygienic point of view. The sensitivity of the method was 2 and 10 ng/ml for ochratoxin A and citrinin, respectively. The recovery rate of the mycotoxins was above 60%.     

哈密黄芪对小鼠的亚急性毒性试验

100只5～6周龄小鼠随机分为5组,每组20只(雌雄各半),雄鼠标记为Ⅰ A～Ⅴ A组,雌鼠标记为Ⅰ B～Ⅴ B组,Ⅰ组为对照组,Ⅱ～Ⅴ组为试验组,分别给小鼠饲喂哈密黄芪干草粉量为基础饲料量15%,30%,45%,60%的混合饲料,连续饲喂5周,记录小鼠体质量、临床症状及主要血液学指标变化,并采集小鼠主要组织器官制作石蜡及透射电镜切片.结果表明,Ⅱ、Ⅲ组小鼠平均日增重为正值,且无明显中毒症状;Ⅳ、Ⅴ组小鼠平均日增重呈负增长,Ⅳ组小鼠饲喂11 d出现明显中毒症状,但5 d后症状减轻或消失,Ⅴ组小鼠饲喂7 d后出现明显中毒症状.Ⅱ～Ⅳ、Ⅴ B组小鼠白细胞总数先升高后降低,而Ⅴ A组持续降低,与对照组相比均有显著差异(P＜0.05);各试验组与对照组相比,红细胞总数及血红蛋白浓度均显著降低(P＜0.05),且降低程度随毒草剂量增加而加剧,各试验组间差异显著(P＜0.05).病理组织学观察可见脑、心脏、肾、脾、睾丸和卵巢等组织发生明显空泡变性.结果提示,哈密黄芪中毒与疯草中毒相似,哈密黄芪应为疯草类植物的一种.     

参金口服液大鼠亚慢性毒性试验研究

为评价参金口服液的安全性,采用Sprague Dawley (SD)大鼠开展了亚慢性毒性试验。120只SD大鼠（雌雄各半）随机分为高、中、低剂量和空白对照组,药物组分别按64、32、16 g /kg体重灌胃给药,空白对照组给予同体积蒸馏水,连续给药28天,停药后观察14天。结果表明,高剂量组出现谷丙转氨酶升高,停药后可恢复正常,其余相关检测指标均未见异常。表明参金口服液在临床应用是安全的。     

Subacute toxicity of dietary T-2 toxin in mice: morphological and hematological effects.

Changes in hematopoietic and lymphoid tissues of young Swiss mice fed a balanced semipurified diet containing T-2 toxin (20 ppm) were examined after one, two, three, four or six weeks. During the first three weeks of exposure of T-2 toxin, lymphoid tissues, bone marrow and splenic red pulp became hypoplastic, resulting in anemia, lymphopenia and eosinopenia. Subsequently, during continued exposure to T-2 toxin, hematopoietic cells regenerated in bone marrow and splenic red pulp and became hyperplastic by six weeks. Granulopoiesis and thrombopoiesis resumed in advance of erythropoiesis. All lymphoid tissues remained atrophic throughout the six week trial. Mice exposed to T-2 toxin also developed perioral dermatitis and hyperkeratosis with ulceration of the mucosa of the esophageal region of the stomach. These results indicated that young mice were susceptible to both the irritant and the hematopoietic-suppressive toxic effects of dietary T-2 toxin. However, supression of hematopoiesis was transient and did not lead to hematopoietic failure.     

Subacute toxicity of Dietary T-2 toxin in mice: influence of protein nutrition.

The subacute toxic effects of dietary T-2 toxin (20 ppm) incorporated in semipurified diets of 8%, 12% or 16% protein, were examined in young Swiss mice after one, two, three and four weeks. Dietary T-2 toxin caused substantial reductions in growth and food consumptaion, the degrees of which were greatest in mice fed the diets of reduced protein content. T-2 toxin consistently caused similar degrees of nonregenerative anemia, lymphopenia, thymic atrophy and gastric hyperkeratosis irrespective of the dietary protein level. However, erythroid hypoplasia was temporary in mice fed T-2 toxin in the 16%-protein diet such that erythroid precursors regenerated in splenic and bone marrow and were hyperplastic after four weeks. Liver to body weight ratios of mice fed T-2 toxin in the 16%-and 12%-protein diets increased during the four week trial in comparison to control mice fed at a similar rate. These observations indicated that suppression of erythropoiesis in mice by dietary T-2 toxin was temporarty and that the interval before regeneration was prolonged by diets of reduced protein content.     

Ethylene glycol toxicosis in a pygmy goat

Ingestion of ethylene glycol was responsible for severe azotemia, acidosis, and abnormal anionic gap value in a pygmy goat. Clinical signs consisted of ataxia, polydipsia, decreased rumen motility, and constipation. Nervous signs included depression, absence of menace response, vertical nystagmus, and terminal convulsions. Four days after onset of clinical signs, antidotal treatment was ineffective. Lesions and oxalate crystals in the kidney were typical of ethylene glycol or plant oxalate toxicosis in other species. Toxicologic analysis revealed ethylene glycol in the rumen content and glycolic acid in urine and ocular fluid.     

Abdominal fat necrosis in a pygmy goat associated with fescue toxicosis.

Abdominal fat necrosis was diagnosed in an 11-year-old female pygmy goat with a 10-day history of lethargy, anorexia, and progressive abdominal distension. Gross necropsy findings revealed multiple firm, dark yellow, nodular masses of fat throughout the abdominal cavity, which compressed several abdominal organs including the rumen, small intestine, spiral colon, and gall bladder. Histologically, multiple to coalescing adipocyte necrosis, saponification, and infiltration with variable numbers of macrophages, lymphocytes, and plasma cells was observed. Fat necrosis in this case was attributed to tall fescue toxicity based on the presence of high levels of endophyte (Neotyphodium coenophialum)-infected fescue identified in the goat's pasture. This is the first known report of abdominal fat necrosis in a goat and demonstrates the fat necrosis syndrome of fescue toxicosis in ruminants.     

Phosphate enema toxicosis in a pygmy goat wether

Phosphate enema toxicity was diagnosed in a 7-month-old, castrated male, pygmy goat. On presentation, clinical findings included mild depression, tachycardia, tachypnea, rumen stasis, muscle tremors, hypocalcemia, hypokalemia, hypochloremia, hyperphosphatemia, azotemia, and metabolic acidosis. Fluid diuresis and parenteral antimicrobial therapy resulted in recovery after 3 d of treatment.     

Toxoplasmosis in a colony of sugar gliders (Petaurus breviceps).

Eleven of a group of 16 sugar gliders died acutely over a period of 2 to 3 weeks. Histopathologic examination revealed a protozoal infection with tachyzoites present in multiple organs, including the intestine, heart, brain, spleen, pancreas, adrenal gland, and kidney. Immunostaining confirmed disseminated toxoplasmosis. Marsupials are susceptible to toxoplasmosis. It was thought that the sugar gliders acquired the infection through foraging in wood chips used as a substrate that were contaminated with feline fecal material.     

Congenital cystic disease of the liver and kidney in a pygmy goat.

A 1-month-old pygmy goat was presented with abdominal distension and hematuria. Anemia, leukocytosis, and increased bilirubin and blood urea nitrogen levels suggested renal and hepatic disease. Radiographs revealed bilateral renomegaly, and ultrasound confirmed bilateral hydronephrosis. Necropsy findings determined that the renomegaly was due in part to edema and marked cystic tubular distension. Similarly, intrahepatic bile ducts were ectatic. The character and distribution of the gross and histologic lesions were consistent with a polycystic disorder, presumably congenital, affecting the liver and the kidney.