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)

To determine whether a model could be established for laboratory investigations, nine squirrel monkeys were inoculated intratracheally with 10(7) median egg-infectious doses of influenza virus type A/New Jersey/8/76 (HSW1N1) (swine influenza virus). They responded with clinically detectable illness including fever, leukopenia, decreased food consumption, increased respiratory rate, occasional coughing, labored breathing, nasal discharge, and lethargy. Convalescence was well advanced by the day 10. All monkeys excreted virus for 7 to 8 days. A scoring procedure (illness score) has been developed for use in studies of vaccine and chemotherapeutic efficacy.
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PMID:Reaction of squirrel monkeys to intratracheal inoculation with influenza/A/New Jersey/76 (swine) virus. 40 21

Squirrel monkeys (Saimiri sciureus) inoculated intratracheally with 10(4.2)-10(8.2) egg median infectious doses (EID50) of type A influenza virus (H3N2) responded with clinical illness including such signs as fever, sneezing or coughing, coryza, and increased respiratory rates. Necropsy studies performed six days after inoculation revealed bronchopneumonia in addition to a mild tracheitis. Squirrel monkeys given 10(5)-6 x 10(8) colony-forming units (cfu) of Streptococcus pneumoniae intratracheally died four to six days later after developing severe illness characterized by fever, bacteremia, lethargy, anorexia, coughing, labored breathing, and bronchopneumonia. Monkeys given 770 cfu of S. pneumoniae responded with less severe symptoms and survived. Four squirrel monkeys inoculated with 10(8.2) EID50 of virus and then 102 hr later with 770 cfu of S. pneumoniae developed severe disease; three of the four animals died within 40 hr. At necropsy these monkeys had more extensive and severe bronchopneumonia than was seen in monkeys infected with either organism alone.
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PMID:Influenza alone and in sequence with pneumonia due to Streptococcus pneumoniae in the squirrel monkey. 2215 62

20 case history interviews with mothers of children younger than 5 and 12 focus groups with young and older mothers, mothers-in-law (grandmothers), traditional birth attendants, spiritual healers, and untrained or semitrained allopaths (village doctors) were conducted in the Matlab in Bangladesh. The qualitative research aimed to examine obstacles to service utilization and community beliefs and practices regarding acute respiratory infections (ARIs) in a rural community where an ARI control project operates. Severe signs and symptoms were more likely to upset mothers than grandmothers. Signs that mothers recognized as severe enough to seek treatment outside the home were labored breathing, chest retractions, lethargy, and inability to feed. Mothers believed that exposure to cold was responsible for pneumonia. Yet, they often thought that an attack by evil influences caused similar illnesses. They refrained from or delayed taking their children with an evil-induced illness for allopathic treatment. Instead, they would seek the services of spiritual healers. Previous experience with a successfully treated case of pneumonia (caused by exposure to cold) was the factor most strongly associated with the decision to seek allopathic treatment. The most common external constraint to bringing children to the Matlab hospital was no one at home to do household work, particularly care for other children. Internal constraints included reluctance to violate purdah and fear of traveling alone. Mothers thought that adhering to purdah kept disease attacks from their children. Mother-blaming attitudes were prevalent, which had a negative effect on mothers' ability to obtain appropriate treatment for ill children.
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PMID:Acute respiratory infections (ARI) in rural Bangladesh: perceptions and practices. 804 Dec 36

The prophylactic effect of in-feed medication of conventional pigs with sulphadimethoxine (SDM), sulphamethoxazole (SMX), and trimethoprim (TMP) was tested by using an Actinobacillus pleuropneumoniae infection model. In each of five experiments, six pigs were given medicated feed twice daily and three pigs received antibiotic-free feed and served as positive (unmedicated, infected) controls. The following drugs or drug combinations were tested (in mg per kg feed): 500 SDM + 100 TMP, 500 SMX + 100 TMP, 125 SMX + 25 TMP, 125 SMX (alone) and 25 TMP (alone). After six days of feed medication, all animals were endobronchially inoculated with A. pleuropneumoniae in a dose of 1-3.10(4) colony-forming units (CFU). The response to the challenge in all control pigs was characterized by fever, lethargy, anorexia, reduced water consumption, and laboured breathing. At autopsy all controls manifested a fibrinous haemorrhagic pleuropneumonia. In-feed medication with 500 SDM + 100 TMP, 500 SMX + 100 TMP as well as 125 SMX + 25 TMP resulted in an effective protection against the challenge in all treated animals. After consumption of feed medicated with 125 mg per kg SMX or 25 mg per kg TMP, pleuropneumonia was evident in all challenged pigs. The results of this study indicate an in vivo potentiation of SMX and TMP in pigs against this respiratory tract pathogen.
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PMID:Prevention of pleuropneumonia in pigs by in-feed medication with sulphadimethoxine and sulphamethoxazole in combination with trimethoprim. 1095 47

A 7-year-old, spayed female mixed breed dog was evaluated for labored breathing, lethargy, and a distended abdomen. Pericardial effusion was diagnosed after radiographic and echocardiographic interpretation. Treatment consisted of thoracocentesis and a single pericardiocentesis. Follow-up examinations indicate that the dog's condition has remained stable.
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PMID:Pericardial effusion in a mixed breed dog. 1170 8

An 11-year-old, spayed female Alaskan malamute with a history of coccidioidal osteomyelitis was evaluated for inappetance and lethargy. Findings included generalized lymphadenopathy, pale mucous membranes, tachycardia, and labored breathing. Laboratory findings and radiographic imaging were consistent with generalized lymphoma and disseminated coccidioidomycosis. Treatment consisted of antibiotics, chemotherapeutic agents, and antifungals.
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PMID:Multicentric lymphoma and disseminated coccidioidomycosis in a dog. 1261 59

Sodium azide is a white crystalline solid used in the manufacture of the explosive lead azide. It is the principal chemical used to generate nitrogen gas in automobile safety airbags and airplane escape chutes and is a broad-spectrum biocide used in both research and agriculture. Toxicology and carcinogenicity studies were conducted by administering sodium azide (greater than 99% pure) in distilled water by gavage to groups of male and female F344/N rats once daily, 5 days per week for 14 days, 13 weeks, or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium and Chinese hamster ovary cells. 14-Day Studies: Rats received 0, 5, 10, 20, 40, or 80 mg/kg sodium azide. All male and female rats receiving 40 or 80 mg/kg and two of five female rats receiving 20 mg/kg died during the first week of the studies. Clinical findings of toxicity included lethargy and inactivity. No grossly observable lesions were present in any of the dose groups. 13-Week Studies: Rats received 0, 1.25, 2.5, 5, 10, or 20 mg/kg sodium azide. Seven of 9 males and all 10 females receiving 20 mg/kg died before the end of the studies. Final mean body weights of treated rats were within 10% of those of the controls. Compound-related clinical findings of toxicity in the 20 mg/kg dose groups included lethargy and labored breathing. Histopathologic lesions induced by sodium azide were limited to the brain (necrosis of the cerebrum and thalamus) and lung (congestion, hemorrhage, and edema), and were observed in rats receiving 20 mg/kg that died during the studies. Body Weights, Feed Consumption, and Survival in the 2-Year Studies: Because compound-related deaths were observed in the groups receiving 20 mg/kg in the 13-week studies, lower dose levels were used in the 2-year studies. Two-year studies were conducted by administering 0, 5, or 10 mg/kg sodium azide to groups of 60 male and 60 female rats. Dose-related depression in mean body weight was observed throughout the study period. Mean feed consumption values in low- and high-dose groups were lower than control values. Survival of high-dose rats of each sex was significantly (P<0.05) lower than controls (males-control, 24/60; low-dose, 27/60; high-dose, 9/60; females-37/60; 43/60; 21/59). The reduced survival was attributed to brain necrosis and cardiovascular collapse induced by sodium azide. Neoplastic and Nonneoplastic Effects in the 2-Year Studies: There were no compound-related increases in incidences of neoplasms in rats. Significantly decreased incidences were observed for certain neoplasms, including mononuclear cell leukemia in male rats (control, 33/60; low-dose, 28/60; high-dose, 14/60), adrenal gland pheochromocytoma in male rats (26/55; 16/56; 6/54), mammary gland fibroadenoma in female rats (20/60; 11/60; 8/59), and pituitary gland neoplasms in female rats (37/60; 28/60; 17/59). These decreases reflected to some extent, but could not be attributed solely to, the reduced survival of the high-dose groups. Compound-related nonneoplastic brain lesions (necrosis of the cerebrum and thalamus) were observed at significantly (P<0.001) increased incidences in high-dose male and female rats. The increased incidence of lung congestion observed in this dose group was considered due to cardiovascular collapse secondary to brain necrosis. Genetic Toxicology: Sodium azide was mutagenic in Salmonella typhimurium strains TA100 and TA1535, with or without exogenous metabolic activation (S9); it was not mutagenic in strain TA1537 or TA98. In cytogenetic tests with Chinese hamster ovary cells, sodium azide induced sister chromatid exchanges, but not chromosomal aberrations, in the presence and the absence of S9. Conclusions: Under the conditions of these 2-year gavage studies, there was no evidence of carcinogenic activity of sodium azide in male or female F344/N rats administered 5 or 10 mg/kg. Sodium azide induced necrosis in the cerebrum and the thalamus of the brain in both male and female rats. Synonyms: Azide, Azium, Smite
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PMID:NTP Toxicology and Carcinogeneis Studies of Sodium Azide (CAS: 26628-22-8) in F344 Rats (Gavage Studies). 1263 70

NTP Toxicology and Carcinogenesis studies of a-methylbenzyl alcohol (greater than 99% pure), a cosmetic ingredient and food flavoring agent, were conducted by administering the chemical in corn oil by gavage to groups of F344/N rats and B6C3F1 mice of each sex for 16 days, 13 weeks, or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium, mouse lymphoma cells, and Chinese hamster ovary (CHO) cells. a-Methylbenzyl alcohol was nominated for study by the National Cancer Institute because of the potential for widespread human exposure. Sixteen-Day and Thirteen-Week Studies: The doses used in the 16-day studies for rats and mice ranged between 125 and 2,000 mg/kg. Six of 10 rats and all mice dosed at 2,000 mg/kg died. In addition, because 7/9 mice dosed at 1,000 mg/kg died, the doses selected for the 13-week studies for mice (47-750 mg/kg) were half those used for rats (93-1,500 mg/kg). In the 13-week studies, deaths of 1/10 male and 3/10 female rats dosed at 1,500 mg/kg were compound related; none of the mice died. Body weight gain was reduced in rats at 1,500 mg/kg; there were no significant histopathologic lesions in either rats or mice. The only compound-related effects were ataxia, labored breathing, and lethargy for up to 30 minutes after dosing in rats and mice given the two highest doses and increases in liver weight to body weight ratios for male rats given the three highest doses and for female rats at all doses. Based on the pattern of mortality and the effects on body weight gain in the short-term studies, doses of 375 and 750 mg/kg a-methylbenzyl alcohol were administered in corn oil by gavage, 5 days per week for 103 weeks, to groups of 50 rats and 50 mice of each sex. Two-Year Studies: Significant reduction in body weight gain commenced at weeks 20-30 in high dose male and female rats, and body weights were 20%-30% below those of vehicle controls at study termination. In the low dose groups, body weight reduction occurred only in male rats during the last 10 weeks of the study. After 80 weeks, 60% of the high dose rats and 80%-100% of the low dose and vehicle control rats were alive; thereafter, the number of deaths in the chemically exposed groups increased sharply so that, at the end of 2 years, final survival for vehicle control, low dose, and high dose rats was 35/50; 8/50; and 1/50 for males and 34/50, 25/50, and 11/50 for females. There were a large number of gavage accidents in these studies (1, 9, and 8 for male rats and 1, 4, and 14 for female rats), but these accidents did not contribute to the increase in mortality after week 80, as all but 4 of these occurred earlier. Mortality in the last quarter of the study was thought to be due to the effects of cumulative toxicity of a-methylbenzyl alcohol on a renal excretory system already compromised by aging. Renal nephropathy that commonly occurs during aging was found in all groups of rats, but the severity was greater in male rats dosed with a-methylbenzyl alcohol. In addition, a collection of nonneoplastic lesions (parathyroid hyperplasia, calcification of the heart and glandular stomach, and fibrous osteodystrophy of bone) was found in the dosed male rats; these lesions were probably secondary to mineral imbalance arising from renal dysfunction. Since survival was poor in low and high dose male and high dose female rats, the sensitivity of the study for detecting a carcinogenic effect in these groups was reduced. Despite this limitation, there were dose-related increases in the incidences of renal tubular cell adenomas or adenocarcinomas (combined) in male rats (vehicle control, 0/50; low dose, 2/50; high dose, 5/50). In addition, transitional cell papillomas of the urinary bladder were observed in one high dose male and two high dose female rats. In mice, a reduction in body weight gain was apparent in the high dose groups of males and females. Final survival rates in mice were similar among groups (male: 39/49; 40/50; 28/50; female: 41/50; 41/50; 38/50). No neoplastic or nonneoplastic lesions were attributed to a-methylbenzyl lesions were attributed to a-methylbenzyl alcohol administration in mice of either sex. Genetic Toxicology: a-Methylbenzyl alcohol was not mutagenic in S. typhimurium strains TA98, TA100, TA1535, or TA1537 when tested in the presence or absence of exogenous metabolic activation. a-Methylbenzyl alcohol produced a positive response without activation in the mouse L5178Y/TK+/- lymphoma assay for induction of trifluorothymidine resistance; it was not tested with activation. In cytogenetic tests with CHO cells, a-methylbenzyl alcohol induced chromosomal aberrations in the presence, but not the absence, of metabolic activation; no induction of sister chromatid exchanges was observed in CHO cells after exposure to a-methylbenzyl alcohol. Conclusions: Under the conditions of these 2-year gavage studies, there was some evidence of carcinogenic activityof a-methylbenzyl alcohol for male F344/N rats, as shown by increased incidences of renal tubular cell adenomas and adenomas or adenocarcinomas (combined). There was no evidence of carcinogenic activity for female F344/N rats administered 375 or 750 mg/kg. Renal toxicity characterized by severe nephropathy and related secondary lesions was observed in the dosed rats, and excessive mortality occurred during the last quarter of the studies. Poor survival reduced the sensitivity of the studies for detecting the presence of a carcinogenic response both in chemically exposed groups of male rats and in the high dose group of female rats. There was no evidence of carcinogenic activity of a-methylbenzyl alcohol for male or female B6C3F1 mice administered 375 or 750 mg/kg for 2 years. Synonyms: styrallyl alcohol; styralyl alcohol; a-methylbenzenemethanol; phenylmethylcarbinol; 1-phenethyl alcohol
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PMID:NTP Toxicology and Carcinogenesis Studies of a-Methylbenzyl Alcohol (CAS No. 98-85-1) in F344/N Rats and B6C3F1 Mice (Gavage Studies). 1269 35

A 9-year-old, male castrated cat was presented with labored breathing and lethargy of 5 d duration. Idiopathic chylothorax was diagnosed based on clinical signs, thoracic radiographs, and thoracentesis. Partial resolution of the pleural effusion followed treatment with rutin, a benzopyrone extracted from plants. The etiology, diagnosis, and treatment of this disease are discussed.
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PMID:The use of rutin in a cat with idiopathic chylothorax. 1618 18

Health monitoring of spotted hyenas (Crocuta crocuta) in the Serengeti ecosystem, Tanzania, revealed Hepatozoon infection in all of 11 immature individuals examined following death from natural causes. Hepatozoon infection was probably an important factor contributing to mortality in two cases that exhibited clinical signs of ataxia, lethargy, ocular discharge, retching, and labored breathing before death. Whether Hepatozoon infection contributed to six deaths from fire, probable lion predation and unknown causes could not be determined. Four deaths from infanticide and starvation were unlikely to be associated with Hepatozoon infection. Histologic examination revealed lung tissue infected with cyst-like structures containing protozoan stages in all eight cases examined and interstitial pneumonia in most cases. Systemic spread of infection to several organs was found in three cases. Alignment of a 426 bp sequence from the parasite's 18s rRNA gene revealed a Hepatozoon species identical to that recently described from two domestic cats in Spain and only 7 bp substitutions when a 853 bp sequence was aligned to this cat Hepatozoon species. Previous reports of infection of wild carnivores in eastern and southern Africa with an unspecified Hepatozoon species similar in appearance to H. canis may have involved the species described in this study.
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PMID:A Hepatozoon species genetically distinct from H. canis infecting spotted hyenas in the Serengeti ecosystem, Tanzania. 1826 20


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