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)

Involvement of the central nervous system (CNS) is common in patients with advanced disease due to human immunodeficiency virus (HIV). Symptoms range from lethargy and apathy to coma, incoordination and ataxia to hemiparesis, loss of memory to severe dementia, and focal to major motor seizures. Involvement may be closely associated with HIV infection per se, as in the AIDS dementia complex, but is frequently caused by opportunistic pathogens such as Toxoplasma gondii and Cryptococcus neoformans or malignancies such as primary lymphoma of the CNS. The clinical presentations of attendant and direct CNS involvement are remarkably non-specific and overlapping, yet a correct diagnosis is critical to successful intervention. Toxoplasmic encephalitis is one of the most common and most treatable causes of AIDS-associated pathology of the CNS. A great deal has been learned in the last 10 years about its unique presentation in the HIV-infected patient with advanced disease. Drs. Benjamin J. Luft of the State University of New York at Stony Brook and Jack S. Remington of the Stanford University School of Medicine and Palo Alto Medical Foundation's Research Institute have studied T. gondii for many years and are two of the leading experts in the field. This commentary comprises an update of their initial review (J Infect Dis 1988;157:1-6) and a presentation of the current approaches to diagnosing and managing toxoplasmic encephalitis in HIV-infected patients.
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PMID:Toxoplasmic encephalitis in AIDS. 152 Jul 57

A seven-year-old male Border Collie was presented with a history of lethargy, episodic circling, incoordination and polydypsia. Physical examination revealed depression, obesity and bradycardia. A neurological examination indicated the possible presence of a space-occupying lesion in the brain. Results of the clinical investigation revealed hyposthenuria, sinus bradycardia and increased concentration of protein in the cerebrospinal fluid. A computerised axial tomography scan revealed a mass in the region of the hypophysis. The dog was euthanased and a post mortem examination confirmed the presence of a craniopharyngioma.
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PMID:A craniopharyngioma in a seven-year-old dog. 194 90

The literature contains about 500 cases of equine leucosis, though the reports are deposited in a great number of journals and vary considerably concerning particular topics. During the last years there has been a remarkable increase of publications about this syndrome in the equine. The clinical leucosis key recommended by us has been confirmed in principle considering the latest literature. In about 70 individual symptoms which can be clinically observed in equine with leucosis 11 can be considered as main symptoms because of their frequency; they are again classified in primary (lymph node tumours including splenomegaly--loss of condition, weakness--cachexia, weight loss, periphery oedema), secondary (anorexia, inappetence--fever--paleness of mucous membrane--anaemia--tachycardia) and accessory (incoordination--tachypnoea, dyspnoea--apathy, lethargy) main symptoms. Furthermore in future it will be necessary to take into more consideration the symptoms "recurrent colic" and "hydrothorax" within differential diagnosis. The main symptom "incoordination" (ataxia, asynergy, paresis, paralysis) is used by us more precisely only in case of impairment of nervous system by neoplastic infiltrations and does not signify as possible symptoms of general physical weakness, for example faltering, staggering, tumbling or lameness. The morphological classification follows further on our previous recommendation. There exist generalized forms with tumour infiltrations in abdominal and in thoracic cavity as well as especially in peripheral lymph nodes. On the other hand there are characteristic manifestations in certain regions of the body, which establish distinctly the clinical symptomatology. They are marked as regional multicentric forms with the main localizations "mediastinal", "splenic", "mesenteric" or "intestinal".(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical diagnostic keys and special manifestations in equine leukosis]. 195 30

Mosquitoes of 3 species (Aedes aegypti, Ae. albopictus, and Culex quinquefasciatus) were fed on human blood containing various concentrations of ivermectin. Three effects (death, decreased egg production, and reduced egg hatching) were observed in the insects, depending upon the concentration of ivermectin ingested. The LD50 of ivermectin in human blood for the 3 mosquito species was estimated to be 126, 208, and 698 ng/ml, respectively. Mosquitoes dying after ingestion of ivermectin developed signs of acute toxicity including paralysis, lethargy, incoordination, and difficulty in movement. Death usually occurred within 48-72 hr. With sublethal blood concentrations of the chemical, mosquitoes survived, but there was a marked reduction in both the number and viability of their eggs. This infertility was only temporary, however, as subsequent refeeding of the insects on uncontaminated blood resulted in the production of normal numbers of fertile eggs. Blood levels of ivermectin which made 50% of the eggs infertile in Ae. aegypti and Ae. albopictus were calculated 3.4 and 4.3 ng/ml, respectively. These latter concentrations of the chemical are within the range found in blood of humans and domestic animals receiving ivermectin for treatment of parasitic infections. This finding suggests that the widespread use of ivermectin in veterinary and human medicine may have an unrecognized effect on mosquito populations.
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PMID:Mortality and infertility in adult mosquitoes after the ingestion of blood containing ivermectin. 222 Dec 16

A 20-month-old girl ingested a maximum of 25 mL of pure methylene iodide. Within two hours, the patient exhibited lethargy and incoordination and vomited. An abdominal radiograph demonstrated the radiopaque material in the gut. In vivo conversion to carbon monoxide was documented with a peak carboxyhemoglobin level of 14.2% reached at 11 hours after ingestion. Two days after ingestion, evidence of hepatotoxicity was apparent, and fulminant hepatic failure quickly ensued. Despite aggressive supportive care and transfer to a liver transplant center, the patient died nine days after ingestion. Methylene iodide ingestion has not been previously reported in human beings. This case verifies that this substance is a potent hepatotoxin, is metabolized to carbon monoxide in vivo, is radiopaque, and may cause bone marrow suppression.
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PMID:Methylene iodide poisoning. 222 24

Two-week repeated-dose and 13-week subchronic studies of HCBD were conducted in B6C3F1 mice. Groups of five mice/sex received 0, 30, 100, 300, 1,000, or 3,000 ppm HCBD in feed for 15 days. Toxic responses, primarily in the higher dose groups, included abnormal clinical signs (lethargy, hunched posture, rough coat, sensitivity to light, and/or incoordination), mortality (all mice in the top two dose groups died by day 7), body and organ weight depression, and gross and histopathological changes. The most prevalent microscopic lesion, seen in all HCBD-treated mice of both sexes, was renal tubular cell necrosis and/or regeneration. Regeneration was seen only in the lower dose groups. Thirteen-week studies were conducted in which groups of 10 mice/sex received 0, 1, 3, 10, 30, or 100 ppm HCBD in feed. No treatment-related clinical signs or mortality were observed. Body weight gain was reduced in the 30- and 100-ppm males (-49 and -56, respectively), and the 100-ppm females (-47). Significant reduction in kidney weights was seen in the 30- and 100-ppm males and 100-ppm females. A treatment-related increase in tubular cell regeneration in the renal cortex occurred in both male and female mice. This lesion was characterized by an increase both in number and basophilic staining intensity of the tubular epithelial cells. Regeneration was seen in the outer stripe of the outer medulla and extended into the medullary rays (pars recta); severity increased with dose. Female mice were more susceptible to the toxicity of HCBD than male mice. Although no adverse effects were observed at the 10-ppm level for male mice in the subchronic study, the regenerative lesion was present in female mice at 1 ppm, the lowest dose administered.
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PMID:Subchronic toxicology studies of hexachloro-1,3-butadiene (HCBD) in B6C3F1 mice by dietary incorporation. 263 70

Within a period of 5 consecutive days after the initial observation of illness was made, 7 of 12 Siberian Husky dogs developed clinical signs of Rickettsia rickettsii infection. One dog died and was necropsied. Clinical signs of infection consisted of lethargy, anorexia, ocular and nasal discharges, and neurologic disorder (incoordination and rolling). Scleral blood vessel injection, fever, lymphadenomegaly, splenomegaly, and increased bronchovesicular lung sounds were prominent findings. Clinical laboratory test results identified decreased platelet numbers, variable neutrophil counts, increased serum alkaline phosphatase activity, hyponatremia, hypokalemia, and bilirubinuria. Diagnosis of Rocky Mountain spotted fever was confirmed by serologic evaluation of acute and convalescent sera, using the micro-immunofluorescence technique, and R rickettsii antigen was determined by demonstration of intracellular rickettsial organisms in vascular endothelial cells of brain and lung (stained with carbol-basic fuchsin and aqueous malachite green) and by demonstration of spotted fever-group rickettsiae in tissues by direct fluorescent antibody technique. Near-simultaneous naturally occurring tick-borne infection of 7 dogs with R rickettsii documents an unreported occurrence.
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PMID:Canine Rocky Mountain spotted fever: a kennel epizootic. 406 17

Recurrent encephalopathy affecting cerebellar and extrapyramidal structures was observed in five members of two families. The syndrome is characterized by sudden onset of truncal ataxia, occasionally accompanied by lethargy and impairment of speech. Choreic and athetoid movements were present, and there was loss of deep tendon reflexes with presence of pathological reflexes. Onset of the disease was early in childhood. Attacks lasted for days to weeks; residual symptoms comprising speech impairment and incoordination were seen in some patients. Both sexes were affected. The pedigrees suggest autosomal dominant inheritance. Pathogenesis remains unexplained by the laboratory studies done; metabolic or immunological processes predisposed by genetic factors are suggested. Similar reports from the literature are discussed; no identical family could be found.
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PMID:Autosomal dominant recurrent encephalopathy of childhood. 685 11

Excessive unexplained mortality was observed in flocks of double-crested cormorants located at Snake Island in Green Bay, Michigan, in June 1992. Clinical signs included weakness, lethargy, diarrhea, respiratory distress, paralysis of the wings and legs, torticollis, and incoordination. The most significant and consistent gross lesions included edema of the eyelids and periocular tissues, pulmonary edema and congestion, marked splenomegaly, hepatic necrosis, and scattered hemorrhages in visceral organs. Histologically, the principal alterations were severe lymphocytic meningoencephalitis and myelitis, as well as splenic lymphoid necrosis with hemorrhage. A type 1 paramyxovirus was isolated from the affected birds and characterized as a velogenic neurotropic strain of Newcastle disease virus. Since the infection occurred in free-living migratory birds, there exists the potential for spread of the virus over a large area, thus posing a hazard to domestic poultry.
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PMID:Neurotropic velogenic Newcastle disease in cormorants in Michigan: pathology and virus characterization. 770 23

Arteether has potent antimalarial activity in vitro against drug resistant Plasmodium falciparum. Preclinical studies of arteether injection have been completed, and phase I safety, tolerance and pharmacokinetic studies are in progress in The Netherlands. No intolerance has yet been observed. Production has been established in a pilot scale in The Netherlands by A.C.F. Beheer BV. Toxicity studies have been conducted in rats and dogs: 3 mg/kg/d for 28 d had no effect. At higher dosages, toxic effects on heart, brain, bone marrow, kidney and liver were observed. Cardiotoxicity is characterized in the dog by a dose-related prolongation of the QTc interval and inversion of the T-wave in some animals. Arrhythmias have not been observed. Electrocardiographic changes returned to baseline values after cessation of daily drug administration. Neuronal toxicity was observed in dogs given daily doses of 6.75 or 15 mg/kg/d intramuscularly for 28 d. Signs of lethargy, incoordination, and abnormal responses appeared in the fourth week. Electroencephalograms exhibited no abnormality. Neuronal degeneration and subsequent myelin degeneration, particularly affecting the cerebellum and other portions of the mid- and hind-brain, were observed. Clinical signs of neurotoxicity did not resolve completely within 30 d after cessation of dosing, and histopathological damage in the brain was still evident. Behavioural and histological evidence of neurotoxicity was also observed in rats. The neurotoxic effects of arteether and artemether in rats and dogs were similar.
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PMID:Role of arteether in the treatment of malaria and plans for further development. 805 28


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