Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Medical records of 34 dogs and 16 cats undergoing surgical repair of diaphragmatic hernia of >2 weeks' duration were reviewed, and long-term follow-up information was obtained. The most common clinical signs were dyspnea and vomiting; however, many of the animals were presented for nonspecific signs such as anorexia, lethargy, and weight loss. Thoracic radiographs revealed evidence of diaphragmatic hernia in only 66% of the animals, and additional imaging tests were often needed to confirm the diagnosis. Thirty-six hernias were repaired through a midline laparotomy; 14 required a median sternotomy combined with a laparotomy. In 14 animals, division of mature adhesions of the lungs or diaphragm to the herniated organs was necessary to permit reduction of the hernia. Fourteen animals required resection of portions of the lungs, liver, or intestine. All hernias were sutured primarily without the use of tissue flaps or mesh implants. Twenty-one of the animals developed transient complications in the postoperative period; the most common of these was pneumothorax. The mortality rate was 14%. Thirty-four (79%) of the animals that were discharged from the hospital had complete resolution of clinical signs, and none developed evidence of recurrent diaphragmatic hernia during the follow-up period. Nine were lost to follow-up.
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PMID:Chronic diaphragmatic hernia in 34 dogs and 16 cats. 1473 6

A seven-year-old flat-coated retriever presented with a history of lethargy, dyspnoea and inappetence of several days' duration. Clinical examination revealed pale mucous membranes and tachypnoea, and haematology demonstrated marked autoagglutination. Thoracic radiographs revealed an increased opacity in the perihilar region. The owners declined further evaluation and the dog was treated symptomatically with immunosuppressive doses of prednisolone and azathioprine. The dog's demeanour improved, although it was eventually euthanased seven weeks later because of dysphagia and worsening dyspnoea. Postmortem examination revealed a widespread, poorly differentiated sarcoma involving the lungs, pericardium, thoracic lymph nodes and spleen. Immune-mediated haemolytic anaemia is a well recognised condition in dogs and is occasionally associated with neoplastic conditions. This is the first case report to describe immune-mediated haemolytic anaemia associated with a diffuse, poorly differentiated sarcoma.
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PMID:Immune-mediated haemolytic anaemia associated with a sarcoma in a flat-coated retriever. 1475 5

A 4.5-year old, male African spur-thighed tortoise (Geochelone sulcata) was presented to the University of Florida Veterinary Teaching Hospital with a 2-week history of lethargy, anorexia, constipation, dyspnea, and coughing up fluid or vomiting. Laboratory results included an inflammatory leukogram and a marked increase in plasma uric acid concentration. Synovial fluid from multiple joints was thick, chalky white, and opaque, with a grainy consistency. Microscopically, the fluid contained numerous brown, needle-like crystals consistent with urates (gout). Gross necropsy findings and histopathology confirmed a diagnosis of systemic gout, with urate deposition, gout tophi, and underlying necrosis in multiple organs, including kidneys, lung, and liver. Dehydration with concurrent renal insufficiency may have impaired urate excretion and led to a build-up of urates in the blood and tissues of this tortoise. A high protein diet also may have contributed to the development of gout. Cytologic evaluation of synovial fluid can be used as a quick and definitive tool to diagnose gout in tortoises.
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PMID:Synovial fluid from an African spur-thighed tortoise (Geochelone sulcata). 1504 27

Vipera palaestinae (Vp), formerly a subspecies of the near east viper Vipera xanthina, is the most common poisonous snake in Israel and neighbouring countries (Jordan, Lebanon and Syria), and is responsible for most envenomations in humans and domestic animals. Hospital records were retrospectively reviewed for confirmed cases of Vp envenomations in dogs over a 13-year period and 327 cases were included in the study. Most envenomations occurred between May and October, and between 02:00 and 10:00 PM. The most frequent clinical signs included: local swelling and oedema (99.6%), viper teeth penetration marks (51%), tachypnoea (50%), panting (44%), increased body temperature (19.2%), tachycardia (>160/min, 19%), salivation (18%) and lameness (15.6%). Common haematological findings included: increased haematocrit (47%), increased haemoglobin concentration (45%), leucocytosis (39%), and thrombocytopenia (30%). The prothrombin time and activated partial thromboplastin time were prolonged in 68 and 21% of the dogs, respectively. Blood biochemistry abnormalities included increased activities of muscle enzymes, hyperglycaemia, hyperbilirubinaemia, hyperglobulinaemia and hypocholesterolaemia. The mortality rate was 4% (13 dogs). The following variables were significantly (p < 0.05) associated with mortality: body weight below 15 kg (p = 0.01), limb envenomation (0.008), envenomation at night (p = 0.025), severe lethargy (P < 0.001), hypothermia (p = 0.04), systemic bleeding (p = 0.001), shock (p = 0.007), dyspnoea (p = 0.002), tachycardia (p = 0.002), thrombocytopenia (p = 0.02), and glucocorticosteroid therapy (p = 0.002). Dogs younger than 4 years had a lower death risk (p = 0.01). The association of steroid therapy with increased mortality suggests that the use of steroids in Vp envenomations may be harmful. Specific antivenom therapy (10 ml/dog) was not associated with a higher survival rate, thus its use, dose and timing of administration should be further investigated.
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PMID:Vipera palaestinae envenomation in 327 dogs: a retrospective cohort study and analysis of risk factors for mortality. 1510 90

Atherosclerosis is a common disease in parrots. The disease is found in all common parrot species, but especially in African Grey parrots and Amazons. It is a disease of older birds that is seen in both males and females. The most common sign is sudden death, but clinical symptoms that can be found include dyspnea, lethargy and nervous signs, such as paresis and collapses. Because the clinical signs are seldomly seen, it is difficult to diagnose atherosclerosis and therefore it is mostly an unexpected finding at necropsy. Age and species are determinants of atherosclerosis in parrots. Suggested risk factors include an elevated plasma cholesterol level, diet composition, social stress and inactivity, but research is needed to confirm this.
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PMID:Atherosclerosis in parrots. A review. 1523 50

Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Endoscopy should be considered if there is persistent vomiting, haematemesis, significant oral burns, severe abdominal pain, dysphagia or stridor. Corticosteroids in high dosage have been recommended if laryngeal and pulmonary oedema supervene, but their value is unproven. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema. Contaminated skin should be washed with copious amounts of water. Skin lesions should be treated as thermal burns; surgery may be required for deep burns. In the case of eye exposure, the affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic may reduce discomfort and assist more thorough decontamination.
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PMID:Hydrogen peroxide poisoning. 1529 93

A 3-yr-old secundiparous female ring-tailed lemur presented to the Auburn University Small Animal Clinic with signs of dyspnea, lethargy, and anorexia. The animal died before she could be examined, and a full necropsy was immediately performed. Provisional necropsy findings included moderate pneumonia and hepatopathy. Acute interstitial pneumonia and focal hepatocellular necrosis were confirmed histologically. Lung impression smears, histopathology, electron microscopy, immunohistochemistry, and tissue culture isolation resulted in a diagnosis of acute disseminated Toxoplasma gondii infection, which was confirmed by polymerase chain reaction. The isolate of T. gondii was avirulent for mice and was named AU Tgl and genetically is type II. The source of the infection remains unclear, but speculation suggests contaminated fruit or blackbirds (Passeriformes: Icteridae) acting as transport hosts for oocysts from nondomestic felids and feral cats on the property.
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PMID:Disseminated toxoplasmosis in a captive ring-tailed lemur (Lemur catta). 1535 1

A 4-year-old German Shepherd was evaluated for progressive depression, lethargy, anorexia, and dyspnea. Despite treatment with diuretics and antibiotics, the dog died. Based on clinical, radiographic, and pathologic findings, the diagnosis was heart failure resulting from aortic valvular endocarditis.
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PMID:Aortic valvular endocarditis in a dog. 1536 43

A 21-month-old, male Pembroke Welsh corgi was referred for investigation of respiratory distress and progressive lethargy. Cardiac evaluation revealed a grade 4 pansystolic murmur over the left and right heart base. A heart murmur, dyspnoea, cyanosis, prolonged capillary refill time and ascites led to the tentative diagnosis of a cardiac malformation with a right-to-left shunt, with likely additional pulmonary disease. Pulmonary hypertension became evident during echocardiography, when the estimated systolic pulmonary artery pressure was over 70 mmHg. Angiography revealed abnormal pulmonary vascular markings consistent with pulmonary hypertension and a small right-to-left shunting patent ductus arteriosus (PDA). The diagnosis of PDA was confirmed at postmortem examination. Histology of the pulmonary arteries showed lesions of plexogenic pulmonary arteriopathy. The question of whether both conditions were separate or part of the same clinical syndrome is discussed in this report.
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PMID:Plexogenic pulmonary arteriopathy in a Pembroke Welsh corgi. 1546 Feb 5

The objectives of this study were to investigate the interactions between Mycoplasma hyopneumoniae and porcine circovirus type 2 (PCV2) and to establish a model for studying the pathogenesis of and testing intervention strategies for the control of PCV2-associated porcine respiratory disease complex (PRDC). Sixty-seven pigs were randomly assigned to four groups. Group 1 (n=17) pigs served as controls, group 2 (n=17) pigs were inoculated with M. hyopneumoniae, group 3 (n=17) pigs were dual infected with M. hyopneumoniae and PCV2, and group 4 (n=16) pigs were inoculated with PCV2. Pigs were inoculated intratracheally with M. hyopneumoniae at 4 weeks of age followed by intranasal inoculation with PCV2 at 6 weeks of age. Dual-infected pigs had moderate dyspnea, lethargy, and reduced weight gain. The overall severity of macroscopic lung lesions, PCV2-associated microscopic lesions in lung and lymphoid tissues, and the amount of PCV2-antigen associated with these lesions were significantly (P <0.05) higher in dual-infected pigs compared with all other groups. Four of 17 (23.5%) dual-infected pigs had decreased growth rate and severe lymphoid depletion and granulomatous lymphadenitis associated with high amounts of PCV2-antigen consistent with postweaning multisystemic wasting syndrome (PMWS). PCV2-antigen in lung tissue was most often associated with M. hyopneumoniae-induced peribronchial lymphoid hyperplasia, suggesting that this is an important site for PCV2 replication in the lung. This study indicates that M. hyopneumoniae potentiates the severity of PCV2-associated lung and lymphoid lesions, increases the amount and prolongs the presence of PCV2-antigen, and increases the incidence of PMWS in pigs.
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PMID:Experimental reproduction of postweaning multisystemic wasting syndrome in pigs by dual infection with Mycoplasma hyopneumoniae and porcine circovirus type 2. 1555 72


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